Is Aluminum Hydroxide Safe In Cosmetics?

Chemistry – Though it may sound similar, aluminum hydroxide is a different compound than the aluminum chlorohydrate commonly used in antiperspirants. Aluminum hydroxide in makeup serves as a pigment, not an antiperspirant or coagulant. While the EWG Skin Deep Cosmetics Database ranks aluminum chlorohydrate at a 3 (moderate hazard), aluminum hydroxide is ranked at 1 (low hazard), the lowest score possible for toxicity risk,

Is aluminum hydroxide safe on skin?

Aluminum hydroxide has no known skin toxicity.

What does aluminum hydroxide do in cosmetics?

Abstract – This is a safety assessment of alumina and aluminum hydroxide as used in cosmetics. Alumina functions as an abrasive, absorbent, anticaking agent, bulking agent, and opacifying agent. Aluminum hydroxide functions as a buffering agent, corrosion inhibitor, and pH adjuster.

• The Food and Drug Administration (FDA) evaluated the safe use of alumina in several medical devices and aluminum hydroxide in over-the-counter drugs, which included a review of human and animal safety data.
• The Cosmetic Ingredient Review (CIR) Expert Panel considered the FDA evaluations as part of the basis for determining the safety of these ingredients as used in cosmetics.

Alumina used in cosmetics is essentially the same as that used in medical devices. This safety assessment does not include metallic or elemental aluminum as a cosmetic ingredient. The CIR Expert Panel concluded that alumina and aluminum hydroxide are safe in the present practices of use and concentration described in this safety assessment.

Is alumina toxic in cosmetics?

It’s been determined safe as used in cosmetics by the independent Cosmetic Ingredient Review panel. It is also approved by the U.S. Food and Drug Administration as a color additive for use in certain over-the-counter drugs.

How toxic is aluminum hydroxide?

Toxicity – Seizures, osteomalacia, and encephalopathy are well-documented toxic effects of aluminum hydroxide. Patients should be asked about any kidney issues before aluminum hydroxide administration, as these outcomes have strong correlations with aluminum hydroxide’s use as a phosphate binder in patients on dialysis.

Is aluminum hydroxide safe in sunscreen?

Scientists at Keele University in Staffordshire have questioned the safety of aluminium added to sunscreens and sunblocks. The researchers, Scott Nicholson, BSc, and Dr Christopher Exley, PhD, Birchall Centre for Inorganic Chemistry and Materials Science at Keele, measured the aluminium content of sunscreens/sunblocks, which either include or do not include an aluminium salt (for example, aluminium hydroxide, aluminium oxide, aluminium silicate, aluminium stearate, aluminium starch octenylsuccinate) as an ingredient.

Aluminium was present in all seven products tested and its content was of particular significance in three products, each of which listed it as an ingredient. Following numerous enquiries the manufacturers were not forthcoming as to the role of aluminium in their product, except one manufacturer, who confirmed that aluminium hydroxide was added to their product to coat the surface and thereby prevent the agglomeration of another ingredient, titanium dioxide particles.

World Health Organisation guidelines recommend a single application of at least 35mL of a sunscreen/sunblock to achieve the stated sun protection factor. For three of the sunscreens/sunblocks investigated a single application of product would result in 200 mg of aluminium being applied to the skin surface.

• In addition, WHO guidelines suggest re-application of product every two hours which, for example, for an average day on the beach, would result in up to 1g of aluminium being applied to the skin surface.
• Skin is permeable to aluminium salts when, for example, they are topically applied as antiperspirant formulations.

It will accumulate in the skin and be transported to sites throughout the body. It is highly likely that the everyday use of sunscreens/sunblocks is an hitherto unrecognised contributor of aluminium to the human body burden of this non-essential metal.

• Perhaps of immediate significance is the potential for aluminium in the skin to act as a pro-oxidant.
• Recent research in the journal Free Radical Biology and Medicine has shown that UV filters in sunscreens promote the formation of reactive oxygen species (ROS) in the nucleated epidermis of the skin.

The authors speculate upon the role which might be played by anti-oxidants, either already in the skin or included in sunscreen formulations, in counteracting the pro-oxidant activities of UV filters though they did not consider how the presence of additional pro-oxidants might exacerbate such effects.

Aluminium is one such pro-oxidant and could significantly increase the potential for oxidative damage in the skin. While the relationship between the burgeoning use of sunscreens/sunblocks and the increased incidence of skin cancers and, in particular, melanoma, is highly controversial it has not hitherto been considered that aluminium in these products could be an extremely significant contributing factor.

Of course, aluminium is already in the skin surface and may not need to be a component of sunscreens/sunblocks to exacerbate oxidative damage attributed to the application of such products.

What is the caution for aluminum hydroxide gel?

Minor (18) –

ascorbic acid ascorbic acid increases levels of aluminum hydroxide by enhancing GI absorption. Applies only to oral form of both agents. Minor/Significance Unknown. aspirin aluminum hydroxide, aspirin. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). aspirin rectal aluminum hydroxide, aspirin rectal. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). aspirin/citric acid/sodium bicarbonate aluminum hydroxide, aspirin/citric acid/sodium bicarbonate. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). balsalazide aluminum hydroxide, balsalazide. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). blessed thistle blessed thistle decreases effects of aluminum hydroxide by pharmacodynamic antagonism. Minor/Significance Unknown. Theoretical interaction. choline magnesium trisalicylate aluminum hydroxide, choline magnesium trisalicylate. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). chromium aluminum hydroxide decreases levels of chromium by inhibition of GI absorption. Applies only to oral form of both agents. Minor/Significance Unknown. Separate by 2 hours. devil’s claw devil’s claw decreases effects of aluminum hydroxide by pharmacodynamic antagonism. Minor/Significance Unknown. diflunisal aluminum hydroxide, diflunisal. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). mesalamine aluminum hydroxide, mesalamine. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). rose hips rose hips increases levels of aluminum hydroxide by enhancing GI absorption. Applies only to oral form of both agents. Minor/Significance Unknown. salicylates (non-asa) aluminum hydroxide, salicylates (non-asa). Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). salsalate aluminum hydroxide, salsalate. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). strontium ranelate aluminum hydroxide decreases levels of strontium ranelate by inhibition of GI absorption. Applies only to oral form of both agents. Minor/Significance Unknown. Separate by 2 hr when possible. sucralfate sucralfate increases levels of aluminum hydroxide by pharmacodynamic synergism. Minor/Significance Unknown. Additive aluminum content. sulfasalazine aluminum hydroxide, sulfasalazine. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). willow bark aluminum hydroxide, willow bark. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid).

acalabrutinib Monitor Closely (1) aluminum hydroxide decreases levels of acalabrutinib by increasing gastric pH. Applies only to oral form of both agents. Modify Therapy/Monitor Closely. Acalabrutinib solubility decreases with increasing gastric pH. Separate dosing by at least 2 hr between administration of antacids and acalabrutinib. acebutolol Monitor Closely (1) aluminum hydroxide decreases levels of acebutolol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. alendronate Monitor Closely (1) aluminum hydroxide decreases levels of alendronate by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. allopurinol Monitor Closely (1) aluminum hydroxide decreases levels of allopurinol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. ascorbic acid Minor (1) ascorbic acid increases levels of aluminum hydroxide by enhancing GI absorption. Applies only to oral form of both agents. Minor/Significance Unknown. aspirin Minor (1) aluminum hydroxide, aspirin. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). aspirin rectal Minor (1) aluminum hydroxide, aspirin rectal. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). aspirin/citric acid/sodium bicarbonate Minor (1) aluminum hydroxide, aspirin/citric acid/sodium bicarbonate. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). atazanavir Serious – Use Alternative (1) aluminum hydroxide will decrease the level or effect of atazanavir by increasing gastric pH. Applies only to oral form of both agents. Avoid or Use Alternate Drug. Atazanavir solubility decreases as pH increases. Reduced plasma concentrations of atazanavir are expected if antacids or buffered medications are coadministered. Administer atazanavir 2 hr before or 1 hr after these medications. atenolol Monitor Closely (1) aluminum hydroxide decreases levels of atenolol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. azithromycin Monitor Closely (1) aluminum hydroxide decreases levels of azithromycin by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. baloxavir marboxil Serious – Use Alternative (1) aluminum hydroxide will decrease the level or effect of baloxavir marboxil by cation binding in GI tract. Avoid or Use Alternate Drug. Baloxavir may bind to polyvalent cations resulting in decreased absorption. Studies in monkeys showed concurrent use with calcium, aluminum, or iron caused significantly decreased plasma levels. Human studies not conducted. balsalazide Minor (1) aluminum hydroxide, balsalazide. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). bearberry Monitor Closely (1) aluminum hydroxide will increase the level or effect of bearberry by passive renal tubular reabsorption – basic urine. Use Caution/Monitor. benazepril Monitor Closely (1) aluminum hydroxide decreases effects of benazepril by unspecified interaction mechanism. Use Caution/Monitor. May decrease absorption. benzphetamine Monitor Closely (1) aluminum hydroxide will increase the level or effect of benzphetamine by passive renal tubular reabsorption – basic urine. Use Caution/Monitor. betaxolol Monitor Closely (1) aluminum hydroxide decreases levels of betaxolol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. bictegravir Monitor Closely (1) aluminum hydroxide will decrease the level or effect of bictegravir by cation binding in GI tract. Modify Therapy/Monitor Closely. Bictegravir can be taken under fasting conditions 2 hr before antacids containing Al, Mg, or Ca. Routine administration of bictegravir simultaneously with, or 2 hr after, antacids containing Al, Mg, or Ca is not recommended. bisoprolol Monitor Closely (1) aluminum hydroxide decreases levels of bisoprolol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. blessed thistle Minor (1) blessed thistle decreases effects of aluminum hydroxide by pharmacodynamic antagonism. Minor/Significance Unknown. Theoretical interaction. bosutinib Monitor Closely (1) aluminum hydroxide decreases levels of bosutinib by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. Bosutinib displays pH-dependent solubility; may use short-acting antacids with administration separated by 2 hr. budesonide Monitor Closely (1) aluminum hydroxide decreases effects of budesonide by increasing gastric pH. Applies only to oral form of both agents. Modify Therapy/Monitor Closely. Enteric-coated budesonide dissolves at pH >5.5. Also, dissolution of extended-release budesonide tablets is pH dependent. Coadministration with drugs that increase gastric pH may cause these budesonide products to prematurely dissolve, and possibly affect release properties and absorption of the drug in the duodenum. cabotegravir Monitor Closely (1) aluminum hydroxide will decrease the level or effect of cabotegravir by cation binding in GI tract. Modify Therapy/Monitor Closely. Administer antacid products at least 2 hr before or 4 hr after taking oral cabotegravir. capecitabine Monitor Closely (1) aluminum hydroxide increases levels of capecitabine by enhancing GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. captopril Monitor Closely (1) aluminum hydroxide decreases effects of captopril by unspecified interaction mechanism. Use Caution/Monitor. Aluminum hydroxide may decrease absorption of captopril. carbonyl iron Monitor Closely (1) aluminum hydroxide will decrease the level or effect of carbonyl iron by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. carvedilol Monitor Closely (1) aluminum hydroxide decreases levels of carvedilol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. cefdinir Monitor Closely (1) aluminum hydroxide will decrease the level or effect of cefdinir by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. cefditoren Monitor Closely (1) aluminum hydroxide will decrease the level or effect of cefditoren by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. cefpodoxime Monitor Closely (1) aluminum hydroxide will decrease the level or effect of cefpodoxime by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. cefuroxime Monitor Closely (1) aluminum hydroxide will decrease the level or effect of cefuroxime by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. celecoxib Monitor Closely (1) aluminum hydroxide decreases levels of celecoxib by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. celiprolol Monitor Closely (1) aluminum hydroxide decreases levels of celiprolol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. chenodiol Monitor Closely (1) aluminum hydroxide decreases levels of chenodiol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. chloroquine Monitor Closely (2) aluminum hydroxide will decrease the level or effect of chloroquine by cation binding in GI tract. Use Caution/Monitor. Separate doses by at least 4 hr aluminum hydroxide will decrease the level or effect of chloroquine by Mechanism: inhibition of GI absorption. Applies only to oral form of both agents. Modify Therapy/Monitor Closely.

cholic acid Monitor Closely (1) aluminum hydroxide will decrease the level or effect of cholic acid by drug binding in GI tract. Use Caution/Monitor. Take cholic acid at least 1 hr before or 4-6 hr (or as great an interval as possible) after a aluminum-based antacid. choline magnesium trisalicylate Minor (1) aluminum hydroxide, choline magnesium trisalicylate. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). chromium Minor (1) aluminum hydroxide decreases levels of chromium by inhibition of GI absorption. Applies only to oral form of both agents. Minor/Significance Unknown. Separate by 2 hours. ciprofloxacin Serious – Use Alternative (1) aluminum hydroxide decreases levels of ciprofloxacin by inhibition of GI absorption. Applies only to oral form of both agents. Avoid or Use Alternate Drug. Separate by 2 hours. crizotinib Monitor Closely (1) aluminum hydroxide decreases levels of crizotinib by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. Drugs that elevate the gastric pH may decrease the solubility of crizotinib and subsequently reduce its bioavailability. However, no formal studies have been conducted., cyclosporine Monitor Closely (1) aluminum hydroxide decreases levels of cyclosporine by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. dabrafenib Monitor Closely (1) aluminum hydroxide will decrease the level or effect of dabrafenib by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. Drugs that alter upper GI tract pH (eg, PPIs, H2-blockers, antacids) may decrease dabrafenib solubility and reduce its bioavailability dapsone Serious – Use Alternative (1) aluminum hydroxide will decrease the level or effect of dapsone by increasing gastric pH. Applies only to oral form of both agents. Avoid or Use Alternate Drug. dasatinib Serious – Use Alternative (1) aluminum hydroxide will decrease the level or effect of dasatinib by increasing gastric pH. Applies only to oral form of both agents. Avoid or Use Alternate Drug. deferasirox Monitor Closely (1) aluminum hydroxide will decrease the level or effect of deferasirox by Other (see comment). Use Caution/Monitor. Avoid combination. Although deferasirox has a lower affinity for aluminum than for iron, do not administer deferasirox with aluminum-containing antacid preparations. deferiprone Monitor Closely (1) aluminum hydroxide decreases levels of deferiprone by enhancing GI absorption. Applies only to oral form of both agents. Modify Therapy/Monitor Closely. Deferiprone may bind polyvalent cations (eg, iron, aluminum, and zinc), separate administration by at least 4 hr between deferiprone and other medications (eg, antacids), or supplements containing these polyvalent cations. deferoxamine Monitor Closely (1) deferoxamine decreases levels of aluminum hydroxide by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Deferoxamine chelates iron; its affinity for other minerals is unknown. delafloxacin Monitor Closely (1) aluminum hydroxide will decrease the level or effect of delafloxacin by cation binding in GI tract. Modify Therapy/Monitor Closely. Oral delafloxacin form chelates with alkaline earth and transition metal cations. Administer oral delafloxacin at least 2 hr before or 6 hr after these agents. demeclocycline Serious – Use Alternative (1) aluminum hydroxide decreases levels of demeclocycline by inhibition of GI absorption. Applies only to oral form of both agents. Avoid or Use Alternate Drug. Separate by 2 hours. devil’s claw Minor (1) devil’s claw decreases effects of aluminum hydroxide by pharmacodynamic antagonism. Minor/Significance Unknown. dextroamphetamine Monitor Closely (1) aluminum hydroxide will increase the level or effect of dextroamphetamine by passive renal tubular reabsorption – basic urine. Use Caution/Monitor. diflunisal Minor (1) aluminum hydroxide, diflunisal. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). digoxin Serious – Use Alternative (1) aluminum hydroxide will increase the level or effect of digoxin by increasing gastric pH. Applies only to oral form of both agents. Avoid or Use Alternate Drug. dolutegravir Monitor Closely (1) aluminum hydroxide will decrease the level or effect of dolutegravir by cation binding in GI tract. Use Caution/Monitor. Administer dolutegravir 2 hr before or 6 hr after taking medications containing polyvalent cations; use alternative therapy if available doxycycline Serious – Use Alternative (1) aluminum hydroxide decreases levels of doxycycline by inhibition of GI absorption. Applies only to oral form of both agents. Avoid or Use Alternate Drug. Separate by 2 hours. eltrombopag Serious – Use Alternative (1) aluminum hydroxide decreases levels of eltrombopag by inhibition of GI absorption. Applies only to oral form of both agents. Contraindicated. Separate by at least 4 hours. elvitegravir Monitor Closely (1) aluminum hydroxide will decrease the level or effect of elvitegravir by cation binding in GI tract. Modify Therapy/Monitor Closely. Elvitegravir plasma concentrations are lower with antacids due to the formation of ionic complexes in the GI tract and not due to changes in gastric pH; separate dose from antacid by at least 2 hr elvitegravir/cobicistat/emtricitabine/tenofovir DF Monitor Closely (1) aluminum hydroxide decreases levels of elvitegravir/cobicistat/emtricitabine/tenofovir DF by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate administration from antacids by 2 hr. enalapril Monitor Closely (1) aluminum hydroxide decreases effects of enalapril by unspecified interaction mechanism. Use Caution/Monitor. ephedrine Monitor Closely (1) aluminum hydroxide will increase the level or effect of ephedrine by passive renal tubular reabsorption – basic urine. Use Caution/Monitor. erythromycin base Monitor Closely (1) aluminum hydroxide increases levels of erythromycin base by unknown mechanism. Use Caution/Monitor. erythromycin ethylsuccinate Monitor Closely (1) aluminum hydroxide increases levels of erythromycin ethylsuccinate by unknown mechanism. Use Caution/Monitor. erythromycin lactobionate Monitor Closely (1) aluminum hydroxide increases levels of erythromycin lactobionate by unknown mechanism. Use Caution/Monitor. erythromycin stearate Monitor Closely (1) aluminum hydroxide increases levels of erythromycin stearate by unknown mechanism. Use Caution/Monitor. esmolol Monitor Closely (1) aluminum hydroxide decreases levels of esmolol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. ethambutol Monitor Closely (1) aluminum hydroxide increases levels of ethambutol by cation binding in GI tract. Use Caution/Monitor. Avoid administering aluminum hydroxide containing antacids for at least 4 hr following ethambutol dose. etidronate Monitor Closely (1) aluminum hydroxide decreases levels of etidronate by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. ferric maltol Monitor Closely (1) aluminum hydroxide will decrease the level or effect of ferric maltol by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. ferrous fumarate Monitor Closely (1) aluminum hydroxide will decrease the level or effect of ferrous fumarate by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. ferrous gluconate Monitor Closely (1) aluminum hydroxide will decrease the level or effect of ferrous gluconate by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. ferrous sulfate Monitor Closely (1) aluminum hydroxide will decrease the level or effect of ferrous sulfate by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. flecainide Monitor Closely (1) aluminum hydroxide will increase the level or effect of flecainide by passive renal tubular reabsorption – basic urine. Use Caution/Monitor. fleroxacin Serious – Use Alternative (1) aluminum hydroxide decreases levels of fleroxacin by inhibition of GI absorption. Applies only to oral form of both agents. Avoid or Use Alternate Drug. Separate by 2 hours. fosamprenavir Monitor Closely (1) aluminum hydroxide will decrease the level or effect of fosamprenavir by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. fosinopril Monitor Closely (1) aluminum hydroxide decreases effects of fosinopril by unspecified interaction mechanism. Use Caution/Monitor. gabapentin Monitor Closely (1) aluminum hydroxide decreases levels of gabapentin by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. gabapentin enacarbil Monitor Closely (1) aluminum hydroxide decreases levels of gabapentin enacarbil by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. gefitinib Monitor Closely (1) aluminum hydroxide decreases levels of gefitinib by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. Separate gefitinib and antacid doses by at least 6 hr. gemifloxacin Serious – Use Alternative (1) aluminum hydroxide decreases levels of gemifloxacin by inhibition of GI absorption. Applies only to oral form of both agents. Avoid or Use Alternate Drug. Separate by 2 hours. glipizide Monitor Closely (1) aluminum hydroxide will increase the level or effect of glipizide by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. glyburide Monitor Closely (1) aluminum hydroxide will increase the level or effect of glyburide by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. ibandronate Monitor Closely (1) aluminum hydroxide decreases levels of ibandronate by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. imidapril Monitor Closely (1) aluminum hydroxide decreases effects of imidapril by unspecified interaction mechanism. Use Caution/Monitor. indinavir Serious – Use Alternative (1) aluminum hydroxide will decrease the level or effect of indinavir by increasing gastric pH. Applies only to oral form of both agents. Avoid or Use Alternate Drug. infigratinib Serious – Use Alternative (1) aluminum hydroxide will decrease the level or effect of infigratinib by inhibition of GI absorption. Applies only to oral form of both agents. Avoid or Use Alternate Drug. If use with an acid-reducing agent cannot be avoided, administer infigratinib 2 hr before and after administration of a locally-acting antacid. iron dextran complex Monitor Closely (1) aluminum hydroxide will decrease the level or effect of iron dextran complex by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. iron sucrose Monitor Closely (1) aluminum hydroxide will decrease the level or effect of iron sucrose by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. isoniazid Monitor Closely (1) aluminum hydroxide decreases levels of isoniazid by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. itraconazole Monitor Closely (1) aluminum hydroxide will decrease the level or effect of itraconazole by inhibition of GI absorption. Applies only to oral form of both agents. Modify Therapy/Monitor Closely. Administer acid neutralizing medicines at least 2 hours before or 2 hours after itraconazole. ketoconazole Monitor Closely (1) aluminum hydroxide decreases levels of ketoconazole by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. Serious – Use Alternative (1) aluminum hydroxide will decrease the level or effect of ketoconazole by increasing gastric pH. Applies only to oral form of both agents. Avoid or Use Alternate Drug. labetalol Monitor Closely (1) aluminum hydroxide decreases levels of labetalol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. lactulose Monitor Closely (1) aluminum hydroxide decreases effects of lactulose by pharmacodynamic antagonism. Use Caution/Monitor. lanthanum carbonate Monitor Closely (1) lanthanum carbonate, aluminum hydroxide. cation binding in GI tract. Use Caution/Monitor. Administer antacid at least 2 hours before or after lanthanum., ledipasvir/sofosbuvir Monitor Closely (1) aluminum hydroxide decreases levels of ledipasvir/sofosbuvir by Other (see comment). Use Caution/Monitor. Comment: Ledipasvir solubility decreases as pH increases; drugs that increase gastric pH are expected to decrease levels of ledipasvir; separate antacid and ledipasivr/sofosbuvir administration by 4 hr. levofloxacin Serious – Use Alternative (1) aluminum hydroxide decreases levels of levofloxacin by inhibition of GI absorption. Applies only to oral form of both agents. Avoid or Use Alternate Drug. Separate by 2 hours. levoketoconazole Monitor Closely (1) aluminum hydroxide decreases levels of levoketoconazole by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. Serious – Use Alternative (1) aluminum hydroxide will decrease the level or effect of levoketoconazole by increasing gastric pH. Applies only to oral form of both agents. Avoid or Use Alternate Drug. lisdexamfetamine Monitor Closely (1) aluminum hydroxide will increase the level or effect of lisdexamfetamine by passive renal tubular reabsorption – basic urine. Use Caution/Monitor. lisinopril Monitor Closely (1) aluminum hydroxide decreases effects of lisinopril by unspecified interaction mechanism. Use Caution/Monitor. memantine Monitor Closely (1) aluminum hydroxide will increase the level or effect of memantine by passive renal tubular reabsorption – basic urine. Use Caution/Monitor. mesalamine Minor (1) aluminum hydroxide, mesalamine. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). methscopolamine Monitor Closely (1) aluminum hydroxide decreases levels of methscopolamine by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. methylphenidate Monitor Closely (1) aluminum hydroxide decreases effects of methylphenidate by enhancing GI absorption. Applies only to oral form of both agents. Modify Therapy/Monitor Closely. Since the characteristics of methylphenidate extended release capsules (Ritalin LA) are pH dependent, coadministration of antacids or acid suppressants could alter the release of methylphenidate. Consider separating the administration of the antacid and the methylphenidate extended-release capsules may be avoided. metoprolol Monitor Closely (1) aluminum hydroxide decreases levels of metoprolol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. mexiletine Monitor Closely (1) aluminum hydroxide will increase the level or effect of mexiletine by passive renal tubular reabsorption – basic urine. Use Caution/Monitor. minocycline Serious – Use Alternative (1) aluminum hydroxide decreases levels of minocycline by inhibition of GI absorption. Applies only to oral form of both agents. Avoid or Use Alternate Drug. Separate by 2 hours. moexipril Monitor Closely (1) aluminum hydroxide decreases effects of moexipril by unspecified interaction mechanism. Use Caution/Monitor. moxifloxacin Serious – Use Alternative (1) aluminum hydroxide decreases levels of moxifloxacin by inhibition of GI absorption. Applies only to oral form of both agents. Avoid or Use Alternate Drug. Separate by 2 hours. mycophenolate Monitor Closely (1) aluminum hydroxide will decrease the level or effect of mycophenolate by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. nadolol Monitor Closely (1) aluminum hydroxide decreases levels of nadolol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. nebivolol Monitor Closely (1) aluminum hydroxide decreases levels of nebivolol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. neratinib Monitor Closely (1) aluminum hydroxide will decrease the level or effect of neratinib by increasing gastric pH. Applies only to oral form of both agents. Modify Therapy/Monitor Closely. Separate antacid and neratinib dosing by 3 hr. nilotinib Monitor Closely (1) aluminum hydroxide decreases levels of nilotinib by increasing gastric pH. Applies only to oral form of both agents. Modify Therapy/Monitor Closely. Avoid this interaction by administering antacids 2 hr after or 2 hr before nilotinib. nimodipine Serious – Use Alternative (1) aluminum hydroxide will increase the level or effect of nimodipine by increasing gastric pH. Applies only to oral form of both agents. Avoid or Use Alternate Drug. nisoldipine Serious – Use Alternative (1) aluminum hydroxide will increase the level or effect of nisoldipine by increasing gastric pH. Applies only to oral form of both agents. Avoid or Use Alternate Drug. nitrendipine Serious – Use Alternative (1) aluminum hydroxide will increase the level or effect of nitrendipine by increasing gastric pH. Applies only to oral form of both agents. Avoid or Use Alternate Drug. nitrofurantoin Monitor Closely (1) aluminum hydroxide decreases levels of nitrofurantoin by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. ofloxacin Serious – Use Alternative (1) aluminum hydroxide decreases levels of ofloxacin by inhibition of GI absorption. Applies only to oral form of both agents. Avoid or Use Alternate Drug. Separate by 2 hours. omadacycline Monitor Closely (1) aluminum hydroxide will decrease the level or effect of omadacycline by inhibition of GI absorption. Applies only to oral form of both agents. Modify Therapy/Monitor Closely. Multivalent cation-containing products may impair absorption of tetracyclines, which may decrease its efficacy. Separate dosing of tetracyclines from these products. oxytetracycline Serious – Use Alternative (1) aluminum hydroxide decreases levels of oxytetracycline by inhibition of GI absorption. Applies only to oral form of both agents. Avoid or Use Alternate Drug. Separate by 2 hours. pamidronate Monitor Closely (1) aluminum hydroxide decreases levels of pamidronate by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. pazopanib Contraindicated (1) aluminum hydroxide will decrease the level or effect of pazopanib by increasing gastric pH. Applies only to oral form of both agents. Contraindicated. Avoid coadministration of pazopanib with drugs that raise gastric pH; may use short-acting antacids in place of PPIs and H2 antagonists, but separate antacid and pazopanib dosing by several hours penbutolol Monitor Closely (1) aluminum hydroxide decreases levels of penbutolol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. penicillamine Monitor Closely (1) aluminum hydroxide decreases levels of penicillamine by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. perindopril Monitor Closely (1) aluminum hydroxide decreases effects of perindopril by unspecified interaction mechanism. Use Caution/Monitor. pexidartinib Monitor Closely (1) aluminum hydroxide will decrease the level or effect of pexidartinib by inhibition of GI absorption. Applies only to oral form of both agents. Modify Therapy/Monitor Closely. Separate pexidartinib by 2 hr before or after taking a locally-acting antacid. pindolol Monitor Closely (1) aluminum hydroxide decreases levels of pindolol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. polysaccharide iron Monitor Closely (1) aluminum hydroxide will decrease the level or effect of polysaccharide iron by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. ponatinib Serious – Use Alternative (1) aluminum hydroxide decreases levels of ponatinib by increasing gastric pH. Applies only to oral form of both agents. Avoid or Use Alternate Drug. posaconazole Monitor Closely (1) aluminum hydroxide will decrease the level or effect of posaconazole by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. propranolol Monitor Closely (1) aluminum hydroxide decreases levels of propranolol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. pseudoephedrine Monitor Closely (1) aluminum hydroxide will increase the level or effect of pseudoephedrine by passive renal tubular reabsorption – basic urine. Use Caution/Monitor. Caution advised with frequent or high dose antacids quinapril Monitor Closely (1) aluminum hydroxide decreases effects of quinapril by unspecified interaction mechanism. Use Caution/Monitor. quinidine Monitor Closely (1) aluminum hydroxide will increase the level or effect of quinidine by passive renal tubular reabsorption – basic urine. Use Caution/Monitor. raltegravir Contraindicated (1) aluminum hydroxide decreases levels of raltegravir by cation binding in GI tract. Contraindicated. Not recommended with or without dose separation. ramipril Monitor Closely (1) aluminum hydroxide decreases effects of ramipril by unspecified interaction mechanism. Use Caution/Monitor. rifampin Monitor Closely (1) aluminum hydroxide will decrease the level or effect of rifampin by Other (see comment). Use Caution/Monitor. Concomitant antacid administration may reduce absorption of rifampin; daily doses of rifampin should be given at least 1 hr before ingestion of antacids rilpivirine Monitor Closely (1) aluminum hydroxide decreases levels of rilpivirine by increasing gastric pH. Applies only to oral form of both agents. Modify Therapy/Monitor Closely. Coadministration of antacids with rilpivirine may cause significant decreases in rilpivirine plasma concentrations because of increased gastric pH. If antacids must be administered, they should be given at least 2 hr before or at least 4 hr after rilpivirine. For the combination product dolutegravir/rilpivirine, antacids should be given at least 4 hr before or at least 6 hr afterwards. riociguat Monitor Closely (1) aluminum hydroxide decreases levels of riociguat by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate administration by at least 1 hour. risedronate Monitor Closely (1) aluminum hydroxide decreases levels of risedronate by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. rose hips Monitor Closely (1) aluminum hydroxide will decrease the level or effect of rose hips by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. Minor (1) rose hips increases levels of aluminum hydroxide by enhancing GI absorption. Applies only to oral form of both agents. Minor/Significance Unknown. rosuvastatin Monitor Closely (1) aluminum hydroxide decreases levels of rosuvastatin by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. salicylates (non-asa) Minor (1) aluminum hydroxide, salicylates (non-asa). Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). salsalate Minor (1) aluminum hydroxide, salsalate. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). sarecycline Monitor Closely (1) aluminum hydroxide will decrease the level or effect of sarecycline by inhibition of GI absorption. Applies only to oral form of both agents. Modify Therapy/Monitor Closely. Multivalent cation-containing products may impair absorption of tetracyclines, which may decrease its efficacy. Separate dosing of tetracyclines from these products. sodium sulfate/?magnesium sulfate/potassium chloride Monitor Closely (1) sodium sulfate/?magnesium sulfate/potassium chloride increases toxicity of aluminum hydroxide by Other (see comment). Use Caution/Monitor. Comment: Coadministration with medications that cause fluid and electrolyte abnormalities may increase the risk of adverse events of seizure, arrhythmias, and renal impairment. sodium sulfate/potassium sulfate/magnesium sulfate Monitor Closely (1) sodium sulfate/potassium sulfate/magnesium sulfate increases toxicity of aluminum hydroxide by Other (see comment). Use Caution/Monitor. Comment: Coadministration with medications that cause fluid and electrolyte abnormalities may increase the risk of adverse events of seizure, arrhythmias, and renal impairment. sofosbuvir/velpatasvir Monitor Closely (1) aluminum hydroxide will decrease the level or effect of sofosbuvir/velpatasvir by increasing gastric pH. Applies only to oral form of both agents. Modify Therapy/Monitor Closely. Velpatasvir solubility decreases as gastric pH increases (practically insoluble at pH >5). Separate administration of sofosbuvir/velpatasvir from antacids by at least 4 hr. sotalol Monitor Closely (1) aluminum hydroxide decreases levels of sotalol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. sotorasib Serious – Use Alternative (1) aluminum hydroxide will decrease the level or effect of sotorasib by inhibition of GI absorption. Applies only to oral form of both agents. Avoid or Use Alternate Drug. If use with an acid-reducing agent cannot be avoided, administer sotorasib 4 hr before or 10 hr after administration of a locally-acting antacid. sparsentan Monitor Closely (1) aluminum hydroxide decreases effects of sparsentan by increasing gastric pH. Applies only to oral form of both agents. Modify Therapy/Monitor Closely. Administer sparsentan 2 hours before or after administration of antacids. Antacids may decrease sparsentan exposure which may reduce efficacy of sparsentan. strontium ranelate Minor (1) aluminum hydroxide decreases levels of strontium ranelate by inhibition of GI absorption. Applies only to oral form of both agents. Minor/Significance Unknown. Separate by 2 hr when possible. sucralfate Minor (1) sucralfate increases levels of aluminum hydroxide by pharmacodynamic synergism. Minor/Significance Unknown. Additive aluminum content. sulfasalazine Minor (1) aluminum hydroxide, sulfasalazine. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). tetracycline Serious – Use Alternative (1) aluminum hydroxide decreases levels of tetracycline by inhibition of GI absorption. Applies only to oral form of both agents. Avoid or Use Alternate Drug. Separate by 2 hours. tiludronate Monitor Closely (1) aluminum hydroxide decreases levels of tiludronate by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. timolol Monitor Closely (1) aluminum hydroxide decreases levels of timolol by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. tolbutamide Monitor Closely (1) aluminum hydroxide will increase the level or effect of tolbutamide by increasing gastric pH. Applies only to oral form of both agents. Use Caution/Monitor. trandolapril Monitor Closely (1) aluminum hydroxide decreases effects of trandolapril by unspecified interaction mechanism. Use Caution/Monitor. ursodiol Monitor Closely (1) aluminum hydroxide decreases effects of ursodiol by pharmacodynamic antagonism. Use Caution/Monitor. vismodegib Monitor Closely (1) aluminum hydroxide will decrease the level or effect of vismodegib by Other (see comment). Use Caution/Monitor. Drugs that increase gastric pH alter vismodegib solubility and therefore reduce bioavailability; effect on efficacy unknown vitamin D Monitor Closely (1) vitamin D increases levels of aluminum hydroxide by Other (see comment). Use Caution/Monitor. Comment: Avoid coadministration. Chronic use of aluminum-containing antacids in conjunction with vitamin D can lead to aluminum retention and possible toxicity. willow bark Minor (1) aluminum hydroxide, willow bark. Mechanism: passive renal tubular reabsorption due to increased pH. Minor/Significance Unknown. Salicylate levels increased at moderate doses; salicylate levels decreased at large doses (d/t increased renal excretion of unchanged salicylic acid). zoledronic acid Monitor Closely (1) aluminum hydroxide decreases levels of zoledronic acid by inhibition of GI absorption. Applies only to oral form of both agents. Use Caution/Monitor. Separate by 2 hours. : AlternaGEL, Amphojel (aluminum hydroxide) dosing, indications, interactions, adverse effects, and more

Is sodium hydroxide safe in beauty products?

– Sodium hydroxide is a pH balancer used in a wide range of beauty and skin care items, like cleansers, soaps, makeup, and creams or lotions. In its pure form, sodium hydroxide is extremely harmful, but beauty and skin care products don’t contain much sodium hydroxide, so they’re safe to use.

Is aluminium absorbed through skin?

Aluminum in therapeutic applications – Antiperspirants: Aluminum compounds have been used commercially in antiperspirants since as early on as in 1903. Due to their antiperspirant effect, aluminum salts are used in dermatology at significantly higher concentrations (10–30% aluminum chlorohydrate) than in over-the-counter antiperspirants.

The German Dermatological Society ( Deutsche Dermatologische Gesellschaft ) considers these to be a simple and suitable treatment option for hyperhidrosis with low side effects ( 2 ). Alternatives in the treatment of hyperhidrosis include tannin preparations with an astringent action, techniques such as tap water iontophoresis, chemical denervation with botulinum toxin A, systemic therapies with antihidrotic agents or psychotropic drugs, as well as surgical procedures ( 2 ).

Although aluminum is absorbed through the skin ( 11, 12 ), the penetration rate of aluminum chlorohydrate following the dermal application of antiperspirants is extremely low at around 0.01% (in two subjects ) and up to 0.06% in pre-damaged skin (in vitro ).

To date, there are no epidemiological studies on internal exposure due to the use of antiperspirants following underarm shaving or the use of hair removal products. Vaccination and hyposensitization: Aluminum salts are used as adjuvants in preparations for vaccines and hyposensitization. The adsorption of antigens on poorly soluble aluminum hydroxide augments the immunological effect ( e5, e6 ).

An aluminum dose of 0.1–0.8 mg is absorbed upon one-off application of a vaccine approved in Europe ( 14 ). Hyposensitization products approved for the German market contain 0.1–1.1 mg aluminum hydroxide per dose. Since these products are usually injected monthly over a 3-year period, aluminum exposure is significantly higher compared with a single vaccination.

Following injection, the aluminum salts become systemically available—the possible risks of this are currently the subject of critical discussion. In 2014, the Paul-Ehrlich Institute classified the “contribution of treatment with aluminum-containing therapeutic allergens to the lifelong accumulation of aluminum in the organism compared with aluminum exposure from other sources as low” and considers it acceptable in view of the therapeutic benefits ( 1 ).

However, data on blood or urine levels in affected patients, which would enable an assessment of the risk of subclinical neurotoxic effects of aluminum, are lacking.

Is Aluminium oxide safe for skin?

Aluminum oxide

Aluminum oxide

* A crystalline compound of Aluminum and Oxygen. Also known as Alumina. Primarily used as an abrasive and thickening agent, but also functions as an anti-caking agent and absorbent. It can be found in cosmetic products like blush, powder foundation, lipstick and facial cleanser.

1. It also acts as an insoluble carrier for mineral pigment, and is frequently mixed into mineral powder makeup.
2. Because of its abrasive texture, many use these crystals to exfoliate and resurface the skin-particularly with Microdermabrasion.
3. A crystalline compound of Aluminum and Oxygen.
4. Also known as Alumina.

Functions: Primarily used as an abrasive and thickening agent, but also functions as an anti-caking agent and absorbent. It can be found in cosmetic products like blush, powder foundation, lipstick and facial cleanser. It also acts as an insoluble carrier for mineral pigment, and is frequently mixed into mineral powder makeup.

• Because of its abrasive texture, many use these crystals to exfoliate and resurface the skin-particularly with,
• Safety Measures/Side Effects: Aluminum Oxide does not penetrate the skin.
• Both the FDA and regard it as safe to use for cosmetic purposes.
• However, it must be noted that aluminum is a neurotoxin.

Studies show toxicty with inhalation or injection ().

Is aluminum and aluminum hydroxide the same thing?

EWG Skin Deep® | What is ALUMINUM HYDROXIDE Data: Fair IMAGE SOURCE: SEARCH PRODUCTS Other Concerns Non-reproductive organ system toxicity (moderate) SYNONYMS ● ALUMINIUM HYDROXIDE SULPHATE ● ALUMINUM HYDROXIDE SULFATE (AL(OH)(SO4)) ● ALUMINUM OXIDE TRIHYDRATE ● ALUMINUM OXIDE, HYDRATE Restricted Restricted: EWG VERIFIED products cannot contain this ingredient without adequate substantiation Aluminum hydroxide, also known as hydrated alumina, is a form of aluminum used as a colorant.

Allergies & Immunotoxicity Developmental and Reproductive Toxicity

EC (Environment Canada).2008. Domestic Substances List Categorization. Canadian Environmental Protection Act (CEPA) Environmental Registry. ED (Environmental Defense).2006. Scorecard _ The Pollution Information Site. http://www.scorecard.org. FDA (U.S. Food and Drug Administration).2008. EAFUS : A Food Additive Database. FDA Office of Food Safety and Applied Nutrition. CIR (Cosmetic Ingredient Review).2006. CIR Compendium, containing abstracts, discussions, and conclusions of CIR cosmetic ingredient safety assessments. Washington DC. NLM (National Library of Medicine).2012. PubMed online scientific bibliography data. http://www.pubmed.gov.

Cosmetics and personal care products are not required to be tested for safety before being allowed on the market. The Skin Deep® scoring system was designed to help the public understand whether a product is safe to use or whether it contains ingredients of concern.

Every product and ingredient in Skin Deep gets a two-part score – one for hazard and one for data availability. The safest products score well by both measures, with a low hazard rating and a fair or better data availability rating. The Skin Deep ingredient hazard score, from 1 to 10, reflects known and suspected hazards linked to the ingredients.

The EWG VERIFIED™ mark means a product meets EWG’s strictest criteria for transparency and health. The Skin Deep data availability rating reflects the number of scientific studies about the product or ingredient in the published scientific literature. NONE LIMITED FAIR GOOD ROBUST Enter the ingredients in EWG’s Build Your Own Report tool to get an approximate score for that product. : EWG Skin Deep® | What is ALUMINUM HYDROXIDE

Is aluminium oxide carcinogenic?

Aluminum has a relatively low toxicity and is not classified according to its carcinogenicity.

Does aluminum hydroxide cause Alzheimer’s?

OCCUPATIONAL EXPOSURE – A meta-analysis of 3 observational studies including more than 1,000 people reported that occupational aluminum dust exposure was not associated with Alzheimer’s, However, further studies that precisely ascertain aluminum exposure are needed.

1. In a more recent 2016 meta-analysis including 4 studies, the relationship between aluminum exposure and dementia was mixed due to the studies being too small,
2. There is no consistent or compelling evidence to associate aluminum with Alzheimer’s disease.
3. Although a few studies have found associations between aluminum levels and Alzheimer’s risk, many others found no such associations.

Due to the inconclusive nature of the findings, it may be advisable to limit excessive exposure.

Virk SA, Eslick GD (2015) Aluminum Levels in Brain, Serum, and Cerebrospinal Fluid are Higher in Alzheimer’s Disease Cases than in Controls: A Series of Meta-Analyses, J Alzheimers Dis 47, 629-638. Killin LO, Starr JM, Shiue IJ et al. (2016) Environmental risk factors for dementia: a systematic review, BMC Geriatr 16, 175. Wang Z, Wei X, Yang J et al. (2016) Chronic exposure to aluminum and risk of Alzheimer’s disease: A meta-analysis, Neurosci Lett 610, 200-206. Cao L, Tan L, Wang HF et al. (2016) Dietary Patterns and Risk of Dementia: a Systematic Review and Meta-Analysis of Cohort Studies, Mol Neurobiol 53, 6144-6154. Dartigues JF, Gagnon M, Michel P et al. (1991), Rev Neurol (Paris) 147, 225-230. Rondeau V, Jacqmin-Gadda H, Commenges D et al. (2009) Aluminum and silica in drinking water and the risk of Alzheimer’s disease or cognitive decline: findings from 15-year follow-up of the PAQUID cohort, Am J Epidemiol 169, 489-496. Flaten TP (1990) Geographical associations between aluminium in drinking water and death rates with dementia (including Alzheimer’s disease), Parkinson’s disease and amyotrophic lateral sclerosis in Norway, Environ Geochem Health 12, 152-167. Forbes WF, Gentleman JF, Maxwell CJ (1995) Concerning the role of aluminum in causing dementia, Exp Gerontol 30, 23-32. Frecker MF (1991) Dementia in Newfoundland: identification of a geographical isolate? J Epidemiol Community Health 45, 307-311. McLachlan DR, Bergeron C, Smith JE et al. (1996) Risk for neuropathologically confirmed Alzheimer’s disease and residual aluminum in municipal drinking water employing weighted residential histories, Neurology 46, 401-405. Neri LC, Hewitt D (1991) Aluminium, Alzheimer’s disease, and drinking water, Lancet 338, 390. Forster DP, Newens AJ, Kay DW et al. (1995) Risk factors in clinically diagnosed presenile dementia of the Alzheimer type: a case-control study in northern England, J Epidemiol Community Health 49, 253-258. Martyn CN, Coggon DN, Inskip H et al. (1997) Aluminum concentrations in drinking water and risk of Alzheimer’s disease, Epidemiology 8, 281-286. Taylor GA, Newens AJ, Edwardson JA et al. (1995) Alzheimer’s disease and the relationship between silicon and aluminium in water supplies in northern England, J Epidemiol Community Health 49, 323-324. Shen XL, Yu JH, Zhang DF et al. (2014) Positive relationship between mortality from Alzheimer’s disease and soil metal concentration in mainland China, J Alzheimers Dis 42, 893-900. Frisardi V, Solfrizzi V, Capurso C et al. (2010) Aluminum in the diet and Alzheimer’s disease: from current epidemiology to possible disease-modifying treatment, J Alzheimers Dis 20, 17-30. Tomljenovic L (2011) Aluminum and Alzheimer’s disease: after a century of controversy, is there a plausible link? J Alzheimers Dis 23, 567-598. Virk SA, Eslick GD (2015) Brief Report: Meta-analysis of Antacid Use and Alzheimer’s Disease: Implications for the Aluminum Hypothesis, Epidemiology 26, 769-773. Mirick DK, Davis S, Thomas DB (2002) Antiperspirant use and the risk of breast cancer, J Natl Cancer Inst 94, 1578-1580. Fakri S, Al-Azzawi A, Al-Tawil N (2006) Antiperspirant use as a risk factor for breast cancer in Iraq, East Mediterr Health J 12, 478-482. McGrath KG (2003) An earlier age of breast cancer diagnosis related to more frequent use of antiperspirants/deodorants and underarm shaving, Eur J Cancer Prev 12, 479-485. Flarend R, Bin T, Elmore D et al. (2001) A preliminary study of the dermal absorption of aluminium from antiperspirants using aluminium-26, Food Chem Toxicol 39, 163-168. Minshall C, Nadal J, Exley C (2014) Aluminium in human sweat, J Trace Elem Med Biol 28, 87-88. Virk SA, Eslick GD (2015) Occupational Exposure to Aluminum and Alzheimer Disease: A Meta-Analysis, J Occup Environ Med 57, 893-896.

Yuko Hara, PhD, is Director of Aging and Alzheimer’s Prevention at the Alzheimer’s Drug Discovery Foundation. Dr. Hara was previously an Assistant Professor in Neuroscience at the Icahn School of Medicine at Mount Sinai, where she remains an adjunct faculty member.

Her research focused on brain aging, specifically how estrogens and reproductive aging influence the aging brain’s synapses and mitochondria. She earned a doctorate in neurology and neuroscience at Weill Graduate School of Medical Sciences of Cornell University and a bachelor’s degree in biology from Cornell University, with additional study at Keio University in Japan.

Dr. Hara has authored numerous peer-reviewed publications, including articles in PNAS and Journal of Neuroscience. Get the latest brain health news: Subscribe

Is aluminum hydroxide bad for your brain?

What Are the Symptoms of Aluminum Hydroxide Toxicity? – Initial adverse effects associated with aluminum hydroxide include;

Nausea, vomiting, and constipation. Lowering of the phosphate to abnormal levels. Chalky taste. Abdominal pain. Pain on urination. Black tarry stools. Mental confusion. Muscle weakness.

When the ingested aluminum hydroxide becomes toxic, the following symptoms occur;

Seizures. Osteomalacia (softening of bones, making them brittle and weak). Encephalopathy (diseases associated with the brain that compromise normal brain functions).

Is aluminum hydroxide FDA approved?

Alumina has been approved by the FDA for use in medical devices.

How do you remove Aluminium hydroxide from your body?

HOW CAN YOU DIAGNOSE AND ELIMINATE EXCESS ALUMINIUM? – First, let’s look at how the body gets rid of excess aluminium. It’s believed that 99% of aluminium consumed in food is removed from the body in the faeces, and only 0.3% is absorbed into the blood, from which it’s then removed by the kidneys.

Unfortunately, this is just a very optimistic hypothesis. The whole process is actually very individual, and depends primarily on the proportion of nutrients in the given body. They’re not permanent, and can vary from person to person. If they’re present in appropriate amounts and proportions, mineral and vitamins have a positive effect on the proper production of enzymes and the process of detoxifying the body, eliminating the harmful effect of aluminium.

In the process of eliminating aluminium from the body, we must ensure the correct level of particularly those elements that are antagonistic to it. These include, for example, silicon. The ratio of zinc to copper is also very important. When it’s correct, the body can effectively defend itself against the effects of this toxic element.

1. Proteins called metallothioneins are responsible for this, and they require efficient methylation.
2. In children who have methylation disorders (most children with autism and neurodevelopmental problems), metallothioneins don’t work properly, and thus are unable to properly adjust the zinc to copper ratio.

The correct ratio of these two elements enables the elimination of heavy metals and aluminium from the body. The right amount of metallothioneins also determines the proper development of the immune system and the nervous system, as well as intestinal health.

• Metallothioneins also participate in the production of hydrochloric acid in the stomach, and affect the perception of the texture and taste of food.
• Many children with eating disorders have disturbed sensory integration and so don’t perceive taste and texture correctly.
• This is related to, among other things, disturbed methylation and a lack of production of the right metallothioneins.

Studies carried out on hair samples to determine the correlation between mineral deficiencies and the body’s toxic load showed a relationship between a deficiency in magnesium and zinc, and elevated levels of mercury and aluminium. Aluminium is infamously in first place among the toxic elements found in children’s bodies.

Various sources state that 17% of autistic children tested have a problem with excess aluminium in the body. In reality, this percentage can be estimated at 90%. This is backed by numerous studies carried out on hair samples of autistic children using the ICP-OES method (inductively coupled plasma optical emission spectrometry), carried out at the Lifeline Diag laboratory.

In autistic children, levels of zinc, magnesium and calcium are almost always lower than normal. To investigate the mineral deficiencies and the degree of the body’s toxic load, including from aluminium, it’s worth performing an, EHA gives a lot more information than just data about the absence or presence of aluminium.

If the result shows a type of metabolism that doesn’t line up with the symptoms of the patient, it can be assumed that the cause of the disorder is an elevated level of heavy metals, usually mercury. We can also check the concentration of toxic elements in the blood, but this method works better with acute poisoning.

We can also perform a diagnostic test of urine or faeces after being exposed to detoxification, e.g. by administering high doses of zinc and selenium. After two or three days, you can check diagnostically whether toxic metals have started leaving the body.

• A diagnostic method used in the United States is also advanced metallothionein profile, where in addition to metallothioneins, the levels of zinc, copper and free copper, ceruloplasmin and glutathione are also tested.
• Only such advanced diagnostics can help define the problem.
• In the case of significant excesses of toxic elements, supplementation is necessary to support the body in the process of detoxification and restoring its biochemical balance.

Effective detoxifiers include B vitamins, zinc and silicon, magnesium malate (the clear leader in aluminium detoxification), spirulina, intestinal sorbents and products supporting detoxification containing extracts of asparagus officinalis root or yucca root.

1. GABA products can also be used as an adjunct to balance the level of glutamate and to increase the amount of gamma-aminobutyric acid naturally present in the brain.
2. At the same time, we need to be aware that detoxification won’t be effective if we don’t take a look at the digestive tract and overcome co-existing gut dysbiosis.

Unfortunately, there’s no panacea that’ll get rid of aluminium on its own. We must approach many factors that enable effective detoxification together. First of all, we need to remove the source of exposure to heavy metals, and at the same time treat gut dysbiosis, which affects the modulation of the immune system. Then, we must eliminate IgG and IgE-dependent allergens from the diet, and supplement it with detoxifying elements. We must also look after the liver, test histamine levels, perform a KPU test (if it’s elevated, we can start to slowly administer vitamin B6, zinc and manganese), and a ceruloplasmin test and, of course, we must restore GABA balance.

To remove aluminium from the body, we must remove organic toxins from the environment, including fungi and moulds that inhibit detoxification. Effective detoxification of the body isn’t possible without efficient methylation. Methylation is the transfer of methyl groups from one substance to another, for example, to activate its decomposition.

For example, methyl groups are needed for the decomposition of histamine. If we have too few methyl groups, we can’t efficiently decompose histamine. Therefore, the histamine level test can help us determine if we methylate well. If we have too little methyl, we have hypomethylation, and serum histamine levels increase; on the other hand, if we have too much methyl, we have hypermethylation, and histamine is usually below normal levels.

To effectively eliminate toxic elements from the body, we can’ forget about proper supplementation. Malic acid, preferably in the form of magnesium malate, works very well for this purpose (plain malic acid also works, but has a slightly weaker effect). Magnesium malate has the ability to bind aluminium and remove it from the body.

Magnesium fills the empty spots that were previously blocked by aluminium, which restores the proper functioning of many enzymes.

Is Aluminium oxide harmful to body?

► Repeated exposure can lead to lung damage. OSHA: The legal airborne permissible exposure limit (PEL) is 5 mg/m3 (as respirable dust) and 15 mg/m3 (as total dust) averaged over an 8-hour workshift.

What are the dangers of aluminum oxide?

UKPID MONOGRAPH ALUMINIUM OXIDE SM Bradberry BSc MB MRCP ST Beer BSc JA Vale MD FRCP FRCPE FRCPG FFOM National Poisons Information Service (Birmingham Centre), West Midlands Poisons Unit, City Hospital NHS Trust, Dudley Road, Birmingham B18 7QH This monograph has been produced by staff of a National Poisons Information Service Centre in the United Kingdom.

The work was commissioned and funded by the UK Departments of Health, and was designed as a source of detailed information for use by poisons information centres. Peer review group: Directors of the UK National Poisons Information Service. ALUMINIUM OXIDE Toxbase summary Type of product Used as a component of paints and varnishes and in the manufacture of alloys, ceramics, glass, electrical insulators and resistors.

Toxicity Significant toxicity has been reported only following chronic occupational inhalation. Features Topical – Aluminium contact sensitivity has been described but is extremely rare. Inhalation – There are no case reports relating to acute exposure.

• Chronic occupational exposure causes conjunctivitis, pharyngitis, and nasal irritation.
• Occupational asthma has been reported in aluminium smelter workers but these individuals are exposed to several other potential allergens (including fluorides and sulphur dioxide).
• Chronic aluminium oxide inhalation may cause pneumoconiosis with cough and exertional dyspnoea, diffuse reticulonodular shadowing on chest X-ray and a restrictive pattern of pulmonary function.

In severe cases death may result from respiratory failure or corpulmonale. – There is evidence from controlled studies among aluminium workers that chronic aluminium oxide exposure with an increased body aluminium burden may be associated with neurocognitive dysfunction but not increased mortality.

1. Management Topical 1.
2. Remove from exposure.2.
3. Treat symptomatically.
4. Inhalation 1.
5. Remove from exposure.2.
6. Give supplemental oxygen by face-mask if there is evidence of respiratory distress.3.
7. Asthmatic symptoms respond to conventional measures.4.
8. In chronic exposure suspected pulmonary fibrosis should be investigated and managed conventionally.5.

Obtain blood and urine for aluminium concentration estimations in symptomatic patients. Discuss with NPIS as these analyses are not widely available.6. Estimation of the aluminium content of CSF may be an important investigation in suspected aluminium-related dementia.7.

• There is no established role for chelation therapy in chronic aluminium oxide poisoning.
• Discuss with NPIS.
• References Bast-Pettersen R, Drablos PA, Goffeng LO, Thomassen Y, Torres CG.
• Neuropsychological deficit among elderly workers in aluminum production.
• Am J Ind Med 1994; 25: 649-62.
• Jederlinic PJ, Abraham JL, Churg A, Himmelstein JS, Epler GR, Gaensler EA.

Pulmonary fibrosis in aluminum oxide workers. Investigation of nine workers, with pathologic examination and microanalysis in three of them. Am Rev Respir Dis 1990; 142: 1179-84. Kongerud J, Boe J, Syseth V, Naalsund A, Magnus P. Aluminium potroom asthma: the Norwegian experience.

Eur Resp J 1994; 7: 165-72. Nielsen J, Dahlqvist M, Welinder H, Thomassen Y, Alexandersson R, Skerfving S. Small airways function in aluminium and stainless steel welders. Int Arch Occup Environ Health 1993; 65: 101-5. Schwarz YA, Kivity S, Fischbein A, Ribak Y, Fireman E, Struhar D, Topilsky M, Greif J.

Eosinophilic lung reaction to aluminium and hard metal. Chest 1994; 105: 1261-3. Sjgren B, Ljunggren KG, Almkvist O, Frech W, Basun H. A follow-up study of five cases of aluminosis. Int Arch Occup Environ Health 1996; 68: 161-4. Substance name Aluminium oxide Origin of substance Occurs naturally as minerals such as bauxite, corundum, diaspore and gibbsite.

CSDS, 1989) Synonyms Aluminium Aluminum Aluminium sesquioxide (CSDS, 1989) Alumina (DOSE, 1992) Chemical group A compound of aluminium, a group III metal. Reference numbers CAS 1344-28-1 (CSDS, 1989) RTECS BD1200000 (RTECS, 1996) UN NIF HAZCHEM CODE NIF Physicochemical properties Chemical structure Aluminium oxide, Al 2 O 3 (DOSE, 1992) Molecular weight 101.96 (DOSE, 1992) Physical state at room temperature Solid (powder) (CSDS, 1989) Colour White (CSDS,1989) Odour NIF Viscosity NA pH NA Solubility Insoluble in water, practically insoluble in non-polar organic solvents, slowly soluble in aqueous alkaline solutions.

(CSDS, 1989) Autoignition temperature NA Chemical interactions Aluminium oxide will react vigorously with vinyl acetate vapour, exothermically with halogenated carbon compounds (above 200C), and exothermically, possibly explosively with oxygen difluoride.

A mixture of aluminium oxide and sodium nitrite will react explosively, and ignition will occur if chlorine trifluoride is mixed with aluminium oxide. Aluminium oxide should be kept well away from water, and is incompatible with strong oxidizers and chlorinated rubber. (CSDS, 1989) Major products of combustion NIF Explosive limits NA Flammability Non-flammable (CSDS, 1989) Boiling point 2977C (CSDS, 1989) Density 4.0 at 20C/4C (DOSE, 1992) Vapour pressure 133.3 Pa at 2158C (CSDS, 1989) Relative vapour density NIF Flash point NA Reactivity NIF Uses Aluminium oxide is used as an adsorbant, desiccant, as a filler for paints and varnishes, and as a catalyst for organic reactions.

Aluminium oxide is employed widely in the manufacture of alloys, ceramics, glass, electrical insulators and resistors. (CSDS, 1989; DOSE, 1992) Hazard/risk classification NIF INTRODUCTION AND EPIDEMIOLOGY Aluminium is the most abundant metal on earth, naturally occurring in rocks as bauxite (aluminium oxide), mica and feldspar (aluminosilicates).

It is a light metal which is a good conductor of both heat and electricity. Aluminium oxide forms as a thin surface layer when aluminium is exposed to air, making it resistant to corrosion. Aluminium oxide is used as an industrial catalyst, adsorbant, desiccant, and as a filler for paints and varnishes.

It is also employed widely in the manufacture of alloys, ceramics, glass, electrical insulators and resistors. Aluminium oxide is an insoluble aluminium compound which does not produce an acute toxic response. The presumed low toxicity of inhaled aluminium oxide led in the past to its use as a prophylactic agent against silicotic lung disease in miners but this practice was abandoned in the 1970’s amid concern that chronic exposure may be harmful.

1. Current important sources of occupational exposure via inhalation are aluminium smelting and welding.
2. MECHANISM OF TOXICITY There is experimental evidence that aluminium inhibits bone mineralization partly by the deposition of aluminium at the osteoid/calcified-bone boundary thereby directly inhibiting calcium influx, and partly by aluminium accumulation in the parathyroid glands with suppression of parathyroid hormone secretion (Visser and Van de Vyver, 1985; Berland et al, 1988; Firling et al, 1994).

Proposed mechanisms of aluminium-induced neurotoxicity include free-radical damage via enhanced lipid peroxidation, impaired glucose metabolism, effects on signal transduction and protein modification and alterations in the axonal transport and phosphorylation state of neurofilaments (Birchall and Chappell, 1988; Exley and Birchall, 1992; Erasmus et al, 1993; Winship, 1993; Haug et al, 1994; Joshi et al, 1994; Strong, 1994).

It has also been suggested that low-level aluminium exposure may influence the body distribution of other essential metals with potential adverse metabolic effects (Rllin et al, 1991). TOXICOKINETICS Absorption In a healthy adult only approximately 15g of the average daily dietary aluminium intake of 3-5mg is absorbed (Winship, 1992).

The intestinal absorption of aluminium and its oxide is enhanced by citrate (which is found frequently in effervescent drug formulations) and reduced by silica. Since aluminium oxide is insoluble it is poorly absorbed following inhalation. Distribution Since aluminium oxide is insoluble some will be retained in the lung following inhalation.

• More than 90 per cent of that which is systematically absorbed is bound to transferrin which does not cross the blood-brain barrier readily.
• The remaining ten per cent is associated with low molecular weight complexes, such as citrate, which can accumulate in brain tissue.
• Systematically absorbed aluminium is stored mainly in bone (up to 40 per cent) and liver.

Excretion Aluminium is excreted predominantly via the kidneys and therefore will accumulate in patients with renal failure (Alfrey, 1980). Following long-term occupational inhalation, aluminium oxide exposed workers with normal renal function may also accumulate aluminium.

In two such cases the total body aluminium half-life was estimated as three years (Elinder et al, 1991). CLINICAL FEATURES: ACUTE EXPOSURE Aluminium oxide ingestion is rare and does not lead to significant toxicological problems; most exposures are via inhalation. No features following acute inhalation have been reported.

CLINICAL FEATURES: CHRONIC EXPOSURE Ocular exposure In one study conjunctivitis was reported significantly more frequently among aluminium welders (n=25) than controls (Nielsen et al, 1993). Dermal exposure Dermal toxicity Thriault et al (1980) described an increased number of skin telangiestases on the upper torso of workers in an aluminium plant.

• There were no associated clinical features and the causative agent was thought to be a hydrocarbon or fluoride emitted from the aluminium electrolytic reactors (Thriault et al, 1980).
• There are reports of contact sensitivity to aluminium but this is extremely rare (Kotovirta et al, 1984).
• Inhalation Pulmonary toxicity Because metallic aluminium has an high affinity for oxygen, exposure to aluminium dust usually also involves exposure to aluminium oxide.

Important sources of such exposure include aluminium smelting (among ‘potroom’ workers) and welders. In some industries sub-micron sized aluminium particles are coated with oil to prevent surface aluminium oxide formation. Removal of this protective coating in vivo however exposes the metal to powerful natural oxidizing agents and tissue damage may result (Dinman, 1987).

1. Smokers are at greater risk of pulmonary complications from aluminium dust as they have a reduced ability to clear inhaled particles from the lungs.
2. In a controlled study of respiratory symptoms among 25 aluminium welders Nielsen et al (1993) reported a significantly increased incidence of pharyngitis.

Interestingly, employees exposed to aluminium/aluminium oxide for less than 2 years were more likely to experience this symptom, possibly reflecting ‘healthy worker’ selection or the development of tolerance. Chronic exposure to stamped aluminium powder (aluminium flake), produced by grinding hard unmelted aluminium, may cause pneumoconiosis.

• Initial symptoms include dyspnoea and cough although in some patients the first clue to respiratory disease is the finding of widespread miliary nodules on chest X-ray (Sjgren et al, 1996a).
• A honeycomb pattern is observed on lung biopsy and lung function tests show a restrictive pattern (Jederlinic et al, 1990).

Patients may develop progressive exertional dyspnoea terminating in respiratory failure or corpulmonale (Mitchell, 1959; Mitchell et al, 1961; Sjgren et al, 1996a). Spontaneous regression is rare and should prompt reconsideration of the diagnosis (Sjgren et al, 1996a).

• Aluminium oxide-induced pulmonary fibrosis may be associated with generalized debility and weight loss (Schwarz et al, 1994).
• Schwarz et al (1994) described a 51 year-old sand-blaster who presented with an eight month history of cough and dyspnoea.
• Chest X-ray showed diffuse bilateral reticulonodular opacities in the mid and lower zones and bronchoalveolar lavage (BAL) fluid analysis revealed a marked eosinophilia (61.6 per cent).

Transbronchial biopsy was consistent with interstitial pneumonia (with a giant-cell infiltrate and dust-laden macrophages). Mineralogic assessment identified large amounts of aluminium silicate and “hard metal”. There was symptomatic and radiological improvement and partial resolution of BAL eosinophilia (to ten per cent) following removal from exposure and three months oral steroid therapy (prednisolone 40mg daily).

1. The authors proposed a multifactorial aetiology in this case involving aluminium, ‘hard metal’ and iron exposure plus idiopathic predisposition.
2. In a controlled study of 14 potroom workers exposed to aluminium oxide for a mean period of 12.9 (SD) 9 years, analysis of bronchoalveolar lavage fluid demonstrated a mild alveolitis (as indicated by altered macrophage activity and increased alveolar capillary permeability) but no evidence of restrictive lung disease (Eklund et al, 1989).

Occupational asthma has been reported in aluminium-smelter (potroom) workers (Kongerud et al, 1990; Saric and Marelja, 1991; Kongerud et al, 1992; Desjardins et al, 1994) but these individuals are exposed to several other allergens including fluorides and sulphur dioxide (Kongerud and Samuelsen, 1991; Syseth and Kongerud, 1992; Kongerud et al, 1992; Kongerud et al, 1994) which makes it difficult to identify a specific aetiological agent.

Neuropsychiatric toxicity There is increasing speculation that Alzheimer’s disease may be linked aetiologically to the accumulation of aluminium in the brain but this remains a highly contentious issue (Ebrahim, 1989; Petit, 1989; Murray et al, 1991; Crapper McLachlan, 1994; Munoz, 1994). Animal studies have demonstrated the ability of aluminium to induce the formation of neurofibrillary tangles (Klatzo et al, 1965), impair the learning ability of rats, and increase brain acetylcholinesterase activity in a similar way to that seen in Alzheimer’s disease (Bilkei-Gorz, 1993).

Other workers have shown elevated aluminium concentrations in brain tissue from patients with Alzheimer’s disease (Crapper et al, 1973) and laser microprobe studies have demonstrated aluminium accumulation in the neurofibrillary tangles of these patients (Good et al, 1992).

1. There is conflicting evidence as to whether neuropsychiatric sequelae result from chronic aluminium oxide exposure.
2. Gibbs (1981) reported no increased mortality from Alzheimer’s disease in over 5000 men employed at an aluminium plant.
3. Clinical examination of 23 workers in an aluminium factory found no neurological signs or symptoms although another man who had worked in the same plant for 13 years died from rapidly progressive encephalopathy (McLaughlin et al, 1962).

Autopsy showed no identifiable cause of death or histological abnormality in the brain but the brain aluminium content was reported to be 20 times higher than normal. Rifat et al (1990) found that although there was no increased incidence of neurological diagnoses in miners exposed between 1944 and 1979 to a mixture of powdered aluminium and aluminium oxide, exposed workers performed significantly less well on cognitive testing than unexposed controls; the likelihood of impairment increased with duration of exposure.

• Bast-Pettersen et al (1994) performed neuropsychological tests on 38 men who had worked for at least ten years in an aluminium production plant.
• Potroom workers had significantly raised urine aluminium concentrations compared to controls; the serum aluminium concentration was normal in all groups.
• Potroom workers also had a significantly increased incidence of subclinical tremor compared to controls with some evidence of impaired visuospatial organization.

In another controlled study of 38 aluminium welders with a median exposure of 7065 hours, a significant dose-related deterioration in certain motor function tests (for example tapping with the non- dominant hand) was observed (Sjgren et al, 1996b). Aluminium exposed workers had urine aluminium concentrations (spot samples) approximately seven times higher than controls.

• Several uncontrolled studies (Sjgren et al, 1990; White et al, 1992; Hnninen et al, 1994) have reported subtle memory defects in aluminium workers.
• Hnninen et al (1994) demonstrated a negative association between short-term memory loss, learning and attention, and the urine aluminium concentration.
• White et al (1992) also found clinical evidence of incoordination in 84 per cent of the 25 workers examined.

Sjgren et al (1994 and 1996a) described a 78 year-old man with a 47 year history of aluminium pneumoconiosis, mild extrapyramidal impairment and moderate dementia. His cerebrospinal fluid aluminium concentration was markedly raised to 259g/L (normal Conclusions Controlled studies among aluminium workers suggest that chronic aluminium/aluminium oxide exposure with an increased body aluminium burden may be associated with neurocognitive dysfunction but not an increased mortality.

• There is insufficient evidence, however, to implicate occupational aluminium oxide exposure in the aetiology of Alzheimer’s disease.
• Bone toxicity Schmid et al (1995) observed increased plasma and urine aluminium concentrations (mean 9.7g/L and 115.8g/L respectively) among 32 aluminium production plant workers (corresponding values among 29 controls were 4.3g/L and 15.5g/L respectively).

There was however no significant difference in lumbar spine bone mineral content (as measured by photon absorptiometry) between the two groups. The authors concluded that occupational aluminium/aluminium oxide exposure did not adversely effect bone density (Schmid et al, 1995).

MANAGEMENT Dermal exposure Dermal manifestations following topical aluminium oxide are rare. If suspected treatment is supportive with removal from exposure. Inhalation Patients with suspected occupational pulmonary toxicity should be removed from exposure, treated symptomatically and undergo a full assessment of respiratory function.

Asthmatic symptoms respond to conventional measures although Saric and Marelja (1991) demonstrated persistent bronchial hyperresponsiveness among potroom workers with occupational asthma (n=30) several years (mean 3.7) following a change of occupation.

Partial resolution of radiographic chest X-ray opacities has been reported following systemic corticosteroid therapy in an aluminium exposed worker with pulmonary fibrosis (Schwarz et al, 1994) but this is unusual. Antidotes Desferrioxamine (deferoxamine) Desferrioxamine forms a stable complex with aluminium and in animal studies it mobilises aluminium primarily from bone with subsequent urinary elimination of the chelate (Gmez et al, 1994; Yokel, 1994).

It is absorbed poorly from the gastrointestinal tract and parenteral therapy is necessary. Theoretically 100mg desferrioxamine can bind 4.1mg aluminium (Winship, 1993). The desferrioxamine chelate is dialyzable and all published clinical studies of aluminium chelation using desferrioxamine involve patients with renal failure undergoing haemodialysis (Sulkova et al, 1991) or, less commonly, peritoneal dialysis (O’Brien et al, 1987) or haemofiltration (Sulkova et al, 1991).

This is discussed in detail in the aluminium sulphate monograph. Sulkova et al (1991) suggested that desferrioxamine-induced aluminium clearance is greater following haemofiltration (mean serum aluminium concentration reduction 66 per cent for 36 filtrations, each a 60 per cent body weight volume exchange) than haemodialysis (mean serum aluminium concentration reduction 41 per cent for 28 five hour dialyses).

Available clinical evidence suggests desferrioxamine therapy can improve aluminium-induced encephalopathy in chronic haemodialysis patients (Day and Ackrill, 1993) and parenteral desferrioxamine therapy may slow the rate of cognitive deterioration in patients with Alzheimer’s disease (Crapper McLachlan et al, 1991; Crapper McLachlan et al, 1993) but there are no data relating to desferrioxamine therapy following aluminium oxide exposure.

If aluminium-induced neurocognitive impairment is confirmed desferrioxamine therapy may have a role. Desferrioxamine and charcoal haemoperfusion Chang and Barre (1983) compared aluminium clearance by desferrioxamine plus charcoal haemoperfusion with desferrioxamine plus haemodialysis in 17 patients with chronic renal failure who were stable on standard haemodialysis.

Neither method enhanced aluminium clearance without desferrioxamine but forty-eight hours after intravenous desferrioxamine charcoal haemoperfusion produced more effective aluminium clearance (mean 65.3 (SD) 11.2 mL/min; n=6) than haemodialysis (mean 44.6 (SD) 13.7mL/min; n=4).

The authors proposed haemoperfusion plus desferrioxamine as an effective method of rapid aluminium elimination in aluminium intoxicated patients to be used in series with haemodialysis in patients with renal failure. There are no data involving patients with aluminium oxide toxicity. Indications In patients exposed to aluminium oxide desferrioxamine therapy could be considered in those with neurocognitive abnormalities associated with a confirmed increased body aluminium burden but there are no clinical data to support this.

Treatment protocol for desferrioxamine This is based on experience with aluminium intoxicated haemodialysis patients and is usually a once weekly intravenous does of 40-80mg/kg. The dose can be reduced to 20-60mg/kg (as indicated by response and adverse effects) if treatment is to be continued for several months (Domingo, 1989).

• Canavese et al (1989) have suggested the therapeutic effectiveness of desferrioxamine may be exhausted after some two years therapy even if aluminium bone deposits persist after this time.
• Adverse effects of desferrioxamine Side-effects of long-term treatment with desferrioxamine include hypotension, gastrointestinal upset, porphyria cutanea tarda-like lesions, transient visual disturbances (McCarthy et al, 1990), posterior cataracts, ototoxicity (Domingo, 1989) and an increased potential for septicaemia, especially Yersinia sepsis (Boyce et al, 1985).

Some dialysis patients with aluminium encephalopathy develop worsening of neurological symptoms within hours of desferrioxamine treatment which may be due to desferrioxamine alone or in combination with a rising plasma aluminium concentration (McCauley and Sorkin, 1989).

1. There are several reports of desferrioxamine-associated systemic fungal infection (mucormycosis) in dialysis patients (Goodill and Abuelo, 1987; Windus et al, 1987).
2. An international registry of this potentially fatal complication has been established (Boelaert et al, 1991) although a causal link between desferrioxamine and fungal infection in these patients has not been confirmed (Vlasveld and van Asbeck, 1991).

Other chelating agents The practical problems of desferrioxamine administration and its side effects have prompted a search for an alternative aluminium chelator although as yet none has been confirmed (Domingo, 1989; Main and Ward, 1992; Yokel, 1994).

Uncontrolled clinical studies with d-penicillamine and dimercaprol in dialysis encephalopathy were unsuccessful (Yokel, 1994) and although in animal studies parenteral citric acid is effective (Domingo et al, 1988), evidence in man that oral citrate enhances gastrointestinal aluminium absorption means the problems of parenteral administration persist.

Rats treated with intraperitoneal aluminium (as the chloride) 2mg/kg daily, four days per week for four weeks, followed by 40mg/kg intraperitoneal ethylenediamine-N,N’-di(2-hydroxyphenyl acetic acid) (EDDHA) showed significantly increased (p Haemodialysis Sulkova et al (1991) reported no aluminium elimination during four haemodialyses without prior desferrioxamine administration.

Peritoneal dialysis Aluminium is removed in small amounts by peritoneal dialysis (O’Brien et al, 1987) and elimination is enhanced by desferrioxamine. In a 32 year-old man with aluminium osteodystrophy O’Brien et al (1987) reported an aluminium clearance of 2.5mL/min with continuous ambulatory peritoneal dialysis (CAPD) alone.

CAPD plus intravenous desferrioxamine (six grams once a week) gave an aluminium clearance of 4.2mL/min compared to a clearance of 3.1mL/min when the same cumulative desferrioxamine dose was given into the peritoneal cavity. Haemofiltration During four haemofiltrations (each with a 60 per cent body weight volume exchange) Sulkova et al (1991) reported a mean 15 per cent fall in the serum aluminium concentration compared to a mean 66 per cent reduction (36 haemofiltrations) in patients pre-treated with desferrioxamine (see above).

Haemoperfusion Chang and Barre (1983) demonstrated that haemoperfusion enhances aluminium elimination only in the presence of desferrioxamine. Protein(transferrin)-bound aluminium is not dialyzable (Day and Ackrill, 1993). Enhancing elimination: Conclusions and recommendations There is currently insufficient data to advocate chelation therapy or extracorporal methods of enhancing elimination in aluminium oxide poisoning.

Most cases involve pulmonary complications following inhalational exposure and should be managed conventionally. The role of chelating agents in the management of neuropsychiatric sequelae remains to be determined. MEDICAL SURVEILLANCE Monitoring airborne aluminium concentrations and periodic assessment of respiratory function are important surveillance measures in the aluminium industry.

Aluminium toxicity should be particularly sought in those who develop unexplained respiratory or neuropsychiatric symptoms. Measurement of blood and urine aluminium concentrations are of some value but close attention must be paid to avoiding sample contamination and consideration given to the potential effect of aluminium-containing medications (House, 1992).

Grouped data are preferable to individual results. The interpretation of urine aluminium concentrations is complicated by the fact that the kinetics of urine aluminium excretion varies depending on the form of aluminium involved (Pierre et al, 1995). Aluminium is evenly distributed between plasma and blood cells so that plasma and whole blood aluminium concentrations have similar value in assessing toxicity (van der Voet and de Wolff, 1985).

Thirteen workers exposed to aluminium flake (‘atomised’ aluminium solid) had significantly higher mean urine (203.6g/L) and blood (12.4g/L) aluminium concentrations compared to controls (median urine and blood concentrations 2.4g/L and less than 2.7g/L respectively) although the higher values in exposed workers were not related to duration of exposure time (Ljunggren et al, 1991).

In the same study the mean urine and blood aluminium concentrations among ten retired workers were 20.0g/L and 3.0g/L respectively. Gitelman et al (1995) observed a strong association between grouped urine aluminium concentrations and airborne occupational exposure but emphasised that individual measurements were not reliable.

1. In a study comparing 84 aluminium smelter workers with 48 controls, significantly higher mean urine aluminium concentrations were observed in workers exposed to airborne aluminium concentrations higher than 0.35mg/m 3 (TLV = 10mg/m 3 ) (Rllin et al, 1996).
2. Urine aluminium monitoring was not useful at lower aluminium exposures, probably because a smaller proportion of the total airborne metal was in the respirable fraction.

Serum aluminium concentrations were less valuable than urinary aluminium as a biological indicator of exposure. Estimation of the aluminium content of cerebrospinal fluid may be important in the investigation of aluminium-related dementia (Sjgren et al, 1994; Sjgren et al, 1996a).

Hair analysis is a poor indicator of aluminium exposure (Wilhelm et al, 1989). AT RISK GROUPS Preterm infants have a limited ability to excrete aluminium. OCCUPATIONAL DATA Occupational exposure standard Long term exposure limit (8 hour TWA reference period) total inhalable dust 10 mg/m 3, respirable dust 5mg/m 3 (Health and Safety Executive, 1995).

OTHER TOXICOLOGICAL DATA Carcinogenicity Workers involved in aluminium production may be at increased risk of developing lung cancer but mortality figures are difficult to interpret, especially when comprehensive occupational and smoking histories are not available (Andersen et al, 1982).

1. Moreover, these workers are exposed to a number of established carcinogens including asbestos, chromium and polycyclic aromatic hydrocarbons (Dufresne et al, 1996).
2. Higher than expected mortality from other cancers, including lymphoreticular and genitourinary malignancies have also been reported (Gibbs, 1981; Rockette and Arena, 1983) but again concomitant exposure to polycyclic aromatic hydrocarbons is likely to be involved (Thriault et al, 1984; Spinelli et al, 1991).

In 521 workers exposed to aluminium oxide in an abrasive manufacturing plant and followed up between 1958 and 1983 Edling et al (1987) found no significantly increased cancer morbidity or mortality. Reprotoxicity NIF Genotoxicity Bacillus subtilis H17 (rec + ), M45 (rec – ) negative DNA damage (DOSE, 1992).

1. Fish toxicity NIF EEC Directive on Drinking Water Quality 80/778/EEC Aluminium: Guide level 0.05mg/L, maximum admissible concentration 0.2g/L (DOSE, 1992).
2. WHO Guidelines for Drinking Water Quality No health-based guideline value is recommended (WHO,1993).
3. AUTHORS SM Bradberry BSc MB MRCP ST Beer BSc JA Vale MD FRCP FRCPE FRCPG FFOM National Poisons Information Service (Birmingham Centre), West Midlands Poisons Unit, City Hospital NHS Trust, Dudley Road, Birmingham B18 7QH UK This monograph was produced by the staff of the Birmingham Centre of the National Poisons Information Service in the United Kingdom.

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• Mitchell J, Manning GB, Molyneux M, Lane RE.
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Adverse Drug React Toxicol Rev 1993; 12: 177-211. Yokel RA. Aluminum chelation: chemistry, clinical, and experimental studies and the search for alternatives to desferrioxamine. J Toxicol Environ Health 1994; 41: 131-74. See Also: Toxicological Abbreviations

Is aluminum hydroxide toxic to humans?

Who Is at Risk for Aluminum Hydroxide Toxicity? – The most common risk factors associated with aluminum hydroxide toxicity include;

People with diminished kidney function. Patients who take aluminum hydroxide as a long-term medication. Working in an area with increased exposure to aluminum. Drug overdose by accident.

Is Aluminium oxide toxic on the skin?

UKPID MONOGRAPH ALUMINIUM OXIDE SM Bradberry BSc MB MRCP ST Beer BSc JA Vale MD FRCP FRCPE FRCPG FFOM National Poisons Information Service (Birmingham Centre), West Midlands Poisons Unit, City Hospital NHS Trust, Dudley Road, Birmingham B18 7QH This monograph has been produced by staff of a National Poisons Information Service Centre in the United Kingdom.

• The work was commissioned and funded by the UK Departments of Health, and was designed as a source of detailed information for use by poisons information centres.
• Peer review group: Directors of the UK National Poisons Information Service.
• ALUMINIUM OXIDE Toxbase summary Type of product Used as a component of paints and varnishes and in the manufacture of alloys, ceramics, glass, electrical insulators and resistors.

Toxicity Significant toxicity has been reported only following chronic occupational inhalation. Features Topical – Aluminium contact sensitivity has been described but is extremely rare. Inhalation – There are no case reports relating to acute exposure.

Chronic occupational exposure causes conjunctivitis, pharyngitis, and nasal irritation. Occupational asthma has been reported in aluminium smelter workers but these individuals are exposed to several other potential allergens (including fluorides and sulphur dioxide). – Chronic aluminium oxide inhalation may cause pneumoconiosis with cough and exertional dyspnoea, diffuse reticulonodular shadowing on chest X-ray and a restrictive pattern of pulmonary function.

In severe cases death may result from respiratory failure or corpulmonale. – There is evidence from controlled studies among aluminium workers that chronic aluminium oxide exposure with an increased body aluminium burden may be associated with neurocognitive dysfunction but not increased mortality.

• Management Topical 1.
• Remove from exposure.2.
• Treat symptomatically.
• Inhalation 1.
• Remove from exposure.2.
• Give supplemental oxygen by face-mask if there is evidence of respiratory distress.3.
• Asthmatic symptoms respond to conventional measures.4.
• In chronic exposure suspected pulmonary fibrosis should be investigated and managed conventionally.5.

Obtain blood and urine for aluminium concentration estimations in symptomatic patients. Discuss with NPIS as these analyses are not widely available.6. Estimation of the aluminium content of CSF may be an important investigation in suspected aluminium-related dementia.7.

• There is no established role for chelation therapy in chronic aluminium oxide poisoning.
• Discuss with NPIS.
• References Bast-Pettersen R, Drablos PA, Goffeng LO, Thomassen Y, Torres CG.
• Neuropsychological deficit among elderly workers in aluminum production.
• Am J Ind Med 1994; 25: 649-62.
• Jederlinic PJ, Abraham JL, Churg A, Himmelstein JS, Epler GR, Gaensler EA.

Pulmonary fibrosis in aluminum oxide workers. Investigation of nine workers, with pathologic examination and microanalysis in three of them. Am Rev Respir Dis 1990; 142: 1179-84. Kongerud J, Boe J, Syseth V, Naalsund A, Magnus P. Aluminium potroom asthma: the Norwegian experience.

• Eur Resp J 1994; 7: 165-72.
• Nielsen J, Dahlqvist M, Welinder H, Thomassen Y, Alexandersson R, Skerfving S.
• Small airways function in aluminium and stainless steel welders.
• Int Arch Occup Environ Health 1993; 65: 101-5.
• Schwarz YA, Kivity S, Fischbein A, Ribak Y, Fireman E, Struhar D, Topilsky M, Greif J.

Eosinophilic lung reaction to aluminium and hard metal. Chest 1994; 105: 1261-3. Sjgren B, Ljunggren KG, Almkvist O, Frech W, Basun H. A follow-up study of five cases of aluminosis. Int Arch Occup Environ Health 1996; 68: 161-4. Substance name Aluminium oxide Origin of substance Occurs naturally as minerals such as bauxite, corundum, diaspore and gibbsite.

• CSDS, 1989) Synonyms Aluminium Aluminum Aluminium sesquioxide (CSDS, 1989) Alumina (DOSE, 1992) Chemical group A compound of aluminium, a group III metal.
• Reference numbers CAS 1344-28-1 (CSDS, 1989) RTECS BD1200000 (RTECS, 1996) UN NIF HAZCHEM CODE NIF Physicochemical properties Chemical structure Aluminium oxide, Al 2 O 3 (DOSE, 1992) Molecular weight 101.96 (DOSE, 1992) Physical state at room temperature Solid (powder) (CSDS, 1989) Colour White (CSDS,1989) Odour NIF Viscosity NA pH NA Solubility Insoluble in water, practically insoluble in non-polar organic solvents, slowly soluble in aqueous alkaline solutions.

(CSDS, 1989) Autoignition temperature NA Chemical interactions Aluminium oxide will react vigorously with vinyl acetate vapour, exothermically with halogenated carbon compounds (above 200C), and exothermically, possibly explosively with oxygen difluoride.

A mixture of aluminium oxide and sodium nitrite will react explosively, and ignition will occur if chlorine trifluoride is mixed with aluminium oxide. Aluminium oxide should be kept well away from water, and is incompatible with strong oxidizers and chlorinated rubber. (CSDS, 1989) Major products of combustion NIF Explosive limits NA Flammability Non-flammable (CSDS, 1989) Boiling point 2977C (CSDS, 1989) Density 4.0 at 20C/4C (DOSE, 1992) Vapour pressure 133.3 Pa at 2158C (CSDS, 1989) Relative vapour density NIF Flash point NA Reactivity NIF Uses Aluminium oxide is used as an adsorbant, desiccant, as a filler for paints and varnishes, and as a catalyst for organic reactions.

Aluminium oxide is employed widely in the manufacture of alloys, ceramics, glass, electrical insulators and resistors. (CSDS, 1989; DOSE, 1992) Hazard/risk classification NIF INTRODUCTION AND EPIDEMIOLOGY Aluminium is the most abundant metal on earth, naturally occurring in rocks as bauxite (aluminium oxide), mica and feldspar (aluminosilicates).

• It is a light metal which is a good conductor of both heat and electricity.
• Aluminium oxide forms as a thin surface layer when aluminium is exposed to air, making it resistant to corrosion.
• Aluminium oxide is used as an industrial catalyst, adsorbant, desiccant, and as a filler for paints and varnishes.

It is also employed widely in the manufacture of alloys, ceramics, glass, electrical insulators and resistors. Aluminium oxide is an insoluble aluminium compound which does not produce an acute toxic response. The presumed low toxicity of inhaled aluminium oxide led in the past to its use as a prophylactic agent against silicotic lung disease in miners but this practice was abandoned in the 1970’s amid concern that chronic exposure may be harmful.

Current important sources of occupational exposure via inhalation are aluminium smelting and welding. MECHANISM OF TOXICITY There is experimental evidence that aluminium inhibits bone mineralization partly by the deposition of aluminium at the osteoid/calcified-bone boundary thereby directly inhibiting calcium influx, and partly by aluminium accumulation in the parathyroid glands with suppression of parathyroid hormone secretion (Visser and Van de Vyver, 1985; Berland et al, 1988; Firling et al, 1994).

Proposed mechanisms of aluminium-induced neurotoxicity include free-radical damage via enhanced lipid peroxidation, impaired glucose metabolism, effects on signal transduction and protein modification and alterations in the axonal transport and phosphorylation state of neurofilaments (Birchall and Chappell, 1988; Exley and Birchall, 1992; Erasmus et al, 1993; Winship, 1993; Haug et al, 1994; Joshi et al, 1994; Strong, 1994).

• It has also been suggested that low-level aluminium exposure may influence the body distribution of other essential metals with potential adverse metabolic effects (Rllin et al, 1991).
• TOXICOKINETICS Absorption In a healthy adult only approximately 15g of the average daily dietary aluminium intake of 3-5mg is absorbed (Winship, 1992).

The intestinal absorption of aluminium and its oxide is enhanced by citrate (which is found frequently in effervescent drug formulations) and reduced by silica. Since aluminium oxide is insoluble it is poorly absorbed following inhalation. Distribution Since aluminium oxide is insoluble some will be retained in the lung following inhalation.

• More than 90 per cent of that which is systematically absorbed is bound to transferrin which does not cross the blood-brain barrier readily.
• The remaining ten per cent is associated with low molecular weight complexes, such as citrate, which can accumulate in brain tissue.
• Systematically absorbed aluminium is stored mainly in bone (up to 40 per cent) and liver.

Excretion Aluminium is excreted predominantly via the kidneys and therefore will accumulate in patients with renal failure (Alfrey, 1980). Following long-term occupational inhalation, aluminium oxide exposed workers with normal renal function may also accumulate aluminium.

In two such cases the total body aluminium half-life was estimated as three years (Elinder et al, 1991). CLINICAL FEATURES: ACUTE EXPOSURE Aluminium oxide ingestion is rare and does not lead to significant toxicological problems; most exposures are via inhalation. No features following acute inhalation have been reported.

CLINICAL FEATURES: CHRONIC EXPOSURE Ocular exposure In one study conjunctivitis was reported significantly more frequently among aluminium welders (n=25) than controls (Nielsen et al, 1993). Dermal exposure Dermal toxicity Thriault et al (1980) described an increased number of skin telangiestases on the upper torso of workers in an aluminium plant.

There were no associated clinical features and the causative agent was thought to be a hydrocarbon or fluoride emitted from the aluminium electrolytic reactors (Thriault et al, 1980). There are reports of contact sensitivity to aluminium but this is extremely rare (Kotovirta et al, 1984). Inhalation Pulmonary toxicity Because metallic aluminium has an high affinity for oxygen, exposure to aluminium dust usually also involves exposure to aluminium oxide.

Important sources of such exposure include aluminium smelting (among ‘potroom’ workers) and welders. In some industries sub-micron sized aluminium particles are coated with oil to prevent surface aluminium oxide formation. Removal of this protective coating in vivo however exposes the metal to powerful natural oxidizing agents and tissue damage may result (Dinman, 1987).

• Smokers are at greater risk of pulmonary complications from aluminium dust as they have a reduced ability to clear inhaled particles from the lungs.
• In a controlled study of respiratory symptoms among 25 aluminium welders Nielsen et al (1993) reported a significantly increased incidence of pharyngitis.

Interestingly, employees exposed to aluminium/aluminium oxide for less than 2 years were more likely to experience this symptom, possibly reflecting ‘healthy worker’ selection or the development of tolerance. Chronic exposure to stamped aluminium powder (aluminium flake), produced by grinding hard unmelted aluminium, may cause pneumoconiosis.

Initial symptoms include dyspnoea and cough although in some patients the first clue to respiratory disease is the finding of widespread miliary nodules on chest X-ray (Sjgren et al, 1996a). A honeycomb pattern is observed on lung biopsy and lung function tests show a restrictive pattern (Jederlinic et al, 1990).

Patients may develop progressive exertional dyspnoea terminating in respiratory failure or corpulmonale (Mitchell, 1959; Mitchell et al, 1961; Sjgren et al, 1996a). Spontaneous regression is rare and should prompt reconsideration of the diagnosis (Sjgren et al, 1996a).

1. Aluminium oxide-induced pulmonary fibrosis may be associated with generalized debility and weight loss (Schwarz et al, 1994).
2. Schwarz et al (1994) described a 51 year-old sand-blaster who presented with an eight month history of cough and dyspnoea.
3. Chest X-ray showed diffuse bilateral reticulonodular opacities in the mid and lower zones and bronchoalveolar lavage (BAL) fluid analysis revealed a marked eosinophilia (61.6 per cent).

Transbronchial biopsy was consistent with interstitial pneumonia (with a giant-cell infiltrate and dust-laden macrophages). Mineralogic assessment identified large amounts of aluminium silicate and “hard metal”. There was symptomatic and radiological improvement and partial resolution of BAL eosinophilia (to ten per cent) following removal from exposure and three months oral steroid therapy (prednisolone 40mg daily).

1. The authors proposed a multifactorial aetiology in this case involving aluminium, ‘hard metal’ and iron exposure plus idiopathic predisposition.
2. In a controlled study of 14 potroom workers exposed to aluminium oxide for a mean period of 12.9 (SD) 9 years, analysis of bronchoalveolar lavage fluid demonstrated a mild alveolitis (as indicated by altered macrophage activity and increased alveolar capillary permeability) but no evidence of restrictive lung disease (Eklund et al, 1989).

Occupational asthma has been reported in aluminium-smelter (potroom) workers (Kongerud et al, 1990; Saric and Marelja, 1991; Kongerud et al, 1992; Desjardins et al, 1994) but these individuals are exposed to several other allergens including fluorides and sulphur dioxide (Kongerud and Samuelsen, 1991; Syseth and Kongerud, 1992; Kongerud et al, 1992; Kongerud et al, 1994) which makes it difficult to identify a specific aetiological agent.

• Neuropsychiatric toxicity There is increasing speculation that Alzheimer’s disease may be linked aetiologically to the accumulation of aluminium in the brain but this remains a highly contentious issue (Ebrahim, 1989; Petit, 1989; Murray et al, 1991; Crapper McLachlan, 1994; Munoz, 1994).
• Animal studies have demonstrated the ability of aluminium to induce the formation of neurofibrillary tangles (Klatzo et al, 1965), impair the learning ability of rats, and increase brain acetylcholinesterase activity in a similar way to that seen in Alzheimer’s disease (Bilkei-Gorz, 1993).

Other workers have shown elevated aluminium concentrations in brain tissue from patients with Alzheimer’s disease (Crapper et al, 1973) and laser microprobe studies have demonstrated aluminium accumulation in the neurofibrillary tangles of these patients (Good et al, 1992).

1. There is conflicting evidence as to whether neuropsychiatric sequelae result from chronic aluminium oxide exposure.
2. Gibbs (1981) reported no increased mortality from Alzheimer’s disease in over 5000 men employed at an aluminium plant.
3. Clinical examination of 23 workers in an aluminium factory found no neurological signs or symptoms although another man who had worked in the same plant for 13 years died from rapidly progressive encephalopathy (McLaughlin et al, 1962).

Autopsy showed no identifiable cause of death or histological abnormality in the brain but the brain aluminium content was reported to be 20 times higher than normal. Rifat et al (1990) found that although there was no increased incidence of neurological diagnoses in miners exposed between 1944 and 1979 to a mixture of powdered aluminium and aluminium oxide, exposed workers performed significantly less well on cognitive testing than unexposed controls; the likelihood of impairment increased with duration of exposure.

Bast-Pettersen et al (1994) performed neuropsychological tests on 38 men who had worked for at least ten years in an aluminium production plant. Potroom workers had significantly raised urine aluminium concentrations compared to controls; the serum aluminium concentration was normal in all groups. Potroom workers also had a significantly increased incidence of subclinical tremor compared to controls with some evidence of impaired visuospatial organization.

In another controlled study of 38 aluminium welders with a median exposure of 7065 hours, a significant dose-related deterioration in certain motor function tests (for example tapping with the non- dominant hand) was observed (Sjgren et al, 1996b). Aluminium exposed workers had urine aluminium concentrations (spot samples) approximately seven times higher than controls.

Several uncontrolled studies (Sjgren et al, 1990; White et al, 1992; Hnninen et al, 1994) have reported subtle memory defects in aluminium workers. Hnninen et al (1994) demonstrated a negative association between short-term memory loss, learning and attention, and the urine aluminium concentration. White et al (1992) also found clinical evidence of incoordination in 84 per cent of the 25 workers examined.

Sjgren et al (1994 and 1996a) described a 78 year-old man with a 47 year history of aluminium pneumoconiosis, mild extrapyramidal impairment and moderate dementia. His cerebrospinal fluid aluminium concentration was markedly raised to 259g/L (normal Conclusions Controlled studies among aluminium workers suggest that chronic aluminium/aluminium oxide exposure with an increased body aluminium burden may be associated with neurocognitive dysfunction but not an increased mortality.

There is insufficient evidence, however, to implicate occupational aluminium oxide exposure in the aetiology of Alzheimer’s disease. Bone toxicity Schmid et al (1995) observed increased plasma and urine aluminium concentrations (mean 9.7g/L and 115.8g/L respectively) among 32 aluminium production plant workers (corresponding values among 29 controls were 4.3g/L and 15.5g/L respectively).

There was however no significant difference in lumbar spine bone mineral content (as measured by photon absorptiometry) between the two groups. The authors concluded that occupational aluminium/aluminium oxide exposure did not adversely effect bone density (Schmid et al, 1995).

MANAGEMENT Dermal exposure Dermal manifestations following topical aluminium oxide are rare. If suspected treatment is supportive with removal from exposure. Inhalation Patients with suspected occupational pulmonary toxicity should be removed from exposure, treated symptomatically and undergo a full assessment of respiratory function.

Asthmatic symptoms respond to conventional measures although Saric and Marelja (1991) demonstrated persistent bronchial hyperresponsiveness among potroom workers with occupational asthma (n=30) several years (mean 3.7) following a change of occupation.

Partial resolution of radiographic chest X-ray opacities has been reported following systemic corticosteroid therapy in an aluminium exposed worker with pulmonary fibrosis (Schwarz et al, 1994) but this is unusual. Antidotes Desferrioxamine (deferoxamine) Desferrioxamine forms a stable complex with aluminium and in animal studies it mobilises aluminium primarily from bone with subsequent urinary elimination of the chelate (Gmez et al, 1994; Yokel, 1994).

It is absorbed poorly from the gastrointestinal tract and parenteral therapy is necessary. Theoretically 100mg desferrioxamine can bind 4.1mg aluminium (Winship, 1993). The desferrioxamine chelate is dialyzable and all published clinical studies of aluminium chelation using desferrioxamine involve patients with renal failure undergoing haemodialysis (Sulkova et al, 1991) or, less commonly, peritoneal dialysis (O’Brien et al, 1987) or haemofiltration (Sulkova et al, 1991).

• This is discussed in detail in the aluminium sulphate monograph.
• Sulkova et al (1991) suggested that desferrioxamine-induced aluminium clearance is greater following haemofiltration (mean serum aluminium concentration reduction 66 per cent for 36 filtrations, each a 60 per cent body weight volume exchange) than haemodialysis (mean serum aluminium concentration reduction 41 per cent for 28 five hour dialyses).

Available clinical evidence suggests desferrioxamine therapy can improve aluminium-induced encephalopathy in chronic haemodialysis patients (Day and Ackrill, 1993) and parenteral desferrioxamine therapy may slow the rate of cognitive deterioration in patients with Alzheimer’s disease (Crapper McLachlan et al, 1991; Crapper McLachlan et al, 1993) but there are no data relating to desferrioxamine therapy following aluminium oxide exposure.

If aluminium-induced neurocognitive impairment is confirmed desferrioxamine therapy may have a role. Desferrioxamine and charcoal haemoperfusion Chang and Barre (1983) compared aluminium clearance by desferrioxamine plus charcoal haemoperfusion with desferrioxamine plus haemodialysis in 17 patients with chronic renal failure who were stable on standard haemodialysis.

Neither method enhanced aluminium clearance without desferrioxamine but forty-eight hours after intravenous desferrioxamine charcoal haemoperfusion produced more effective aluminium clearance (mean 65.3 (SD) 11.2 mL/min; n=6) than haemodialysis (mean 44.6 (SD) 13.7mL/min; n=4).

1. The authors proposed haemoperfusion plus desferrioxamine as an effective method of rapid aluminium elimination in aluminium intoxicated patients to be used in series with haemodialysis in patients with renal failure.
2. There are no data involving patients with aluminium oxide toxicity.
3. Indications In patients exposed to aluminium oxide desferrioxamine therapy could be considered in those with neurocognitive abnormalities associated with a confirmed increased body aluminium burden but there are no clinical data to support this.

Treatment protocol for desferrioxamine This is based on experience with aluminium intoxicated haemodialysis patients and is usually a once weekly intravenous does of 40-80mg/kg. The dose can be reduced to 20-60mg/kg (as indicated by response and adverse effects) if treatment is to be continued for several months (Domingo, 1989).

• Canavese et al (1989) have suggested the therapeutic effectiveness of desferrioxamine may be exhausted after some two years therapy even if aluminium bone deposits persist after this time.
• Adverse effects of desferrioxamine Side-effects of long-term treatment with desferrioxamine include hypotension, gastrointestinal upset, porphyria cutanea tarda-like lesions, transient visual disturbances (McCarthy et al, 1990), posterior cataracts, ototoxicity (Domingo, 1989) and an increased potential for septicaemia, especially Yersinia sepsis (Boyce et al, 1985).

Some dialysis patients with aluminium encephalopathy develop worsening of neurological symptoms within hours of desferrioxamine treatment which may be due to desferrioxamine alone or in combination with a rising plasma aluminium concentration (McCauley and Sorkin, 1989).

1. There are several reports of desferrioxamine-associated systemic fungal infection (mucormycosis) in dialysis patients (Goodill and Abuelo, 1987; Windus et al, 1987).
2. An international registry of this potentially fatal complication has been established (Boelaert et al, 1991) although a causal link between desferrioxamine and fungal infection in these patients has not been confirmed (Vlasveld and van Asbeck, 1991).

Other chelating agents The practical problems of desferrioxamine administration and its side effects have prompted a search for an alternative aluminium chelator although as yet none has been confirmed (Domingo, 1989; Main and Ward, 1992; Yokel, 1994).

Uncontrolled clinical studies with d-penicillamine and dimercaprol in dialysis encephalopathy were unsuccessful (Yokel, 1994) and although in animal studies parenteral citric acid is effective (Domingo et al, 1988), evidence in man that oral citrate enhances gastrointestinal aluminium absorption means the problems of parenteral administration persist.

Rats treated with intraperitoneal aluminium (as the chloride) 2mg/kg daily, four days per week for four weeks, followed by 40mg/kg intraperitoneal ethylenediamine-N,N’-di(2-hydroxyphenyl acetic acid) (EDDHA) showed significantly increased (p Haemodialysis Sulkova et al (1991) reported no aluminium elimination during four haemodialyses without prior desferrioxamine administration.

Peritoneal dialysis Aluminium is removed in small amounts by peritoneal dialysis (O’Brien et al, 1987) and elimination is enhanced by desferrioxamine. In a 32 year-old man with aluminium osteodystrophy O’Brien et al (1987) reported an aluminium clearance of 2.5mL/min with continuous ambulatory peritoneal dialysis (CAPD) alone.

CAPD plus intravenous desferrioxamine (six grams once a week) gave an aluminium clearance of 4.2mL/min compared to a clearance of 3.1mL/min when the same cumulative desferrioxamine dose was given into the peritoneal cavity. Haemofiltration During four haemofiltrations (each with a 60 per cent body weight volume exchange) Sulkova et al (1991) reported a mean 15 per cent fall in the serum aluminium concentration compared to a mean 66 per cent reduction (36 haemofiltrations) in patients pre-treated with desferrioxamine (see above).

1. Haemoperfusion Chang and Barre (1983) demonstrated that haemoperfusion enhances aluminium elimination only in the presence of desferrioxamine.
2. Protein(transferrin)-bound aluminium is not dialyzable (Day and Ackrill, 1993).
3. Enhancing elimination: Conclusions and recommendations There is currently insufficient data to advocate chelation therapy or extracorporal methods of enhancing elimination in aluminium oxide poisoning.

Most cases involve pulmonary complications following inhalational exposure and should be managed conventionally. The role of chelating agents in the management of neuropsychiatric sequelae remains to be determined. MEDICAL SURVEILLANCE Monitoring airborne aluminium concentrations and periodic assessment of respiratory function are important surveillance measures in the aluminium industry.

• Aluminium toxicity should be particularly sought in those who develop unexplained respiratory or neuropsychiatric symptoms.
• Measurement of blood and urine aluminium concentrations are of some value but close attention must be paid to avoiding sample contamination and consideration given to the potential effect of aluminium-containing medications (House, 1992).

Grouped data are preferable to individual results. The interpretation of urine aluminium concentrations is complicated by the fact that the kinetics of urine aluminium excretion varies depending on the form of aluminium involved (Pierre et al, 1995). Aluminium is evenly distributed between plasma and blood cells so that plasma and whole blood aluminium concentrations have similar value in assessing toxicity (van der Voet and de Wolff, 1985).

Thirteen workers exposed to aluminium flake (‘atomised’ aluminium solid) had significantly higher mean urine (203.6g/L) and blood (12.4g/L) aluminium concentrations compared to controls (median urine and blood concentrations 2.4g/L and less than 2.7g/L respectively) although the higher values in exposed workers were not related to duration of exposure time (Ljunggren et al, 1991).

In the same study the mean urine and blood aluminium concentrations among ten retired workers were 20.0g/L and 3.0g/L respectively. Gitelman et al (1995) observed a strong association between grouped urine aluminium concentrations and airborne occupational exposure but emphasised that individual measurements were not reliable.

• In a study comparing 84 aluminium smelter workers with 48 controls, significantly higher mean urine aluminium concentrations were observed in workers exposed to airborne aluminium concentrations higher than 0.35mg/m 3 (TLV = 10mg/m 3 ) (Rllin et al, 1996).
• Urine aluminium monitoring was not useful at lower aluminium exposures, probably because a smaller proportion of the total airborne metal was in the respirable fraction.

Serum aluminium concentrations were less valuable than urinary aluminium as a biological indicator of exposure. Estimation of the aluminium content of cerebrospinal fluid may be important in the investigation of aluminium-related dementia (Sjgren et al, 1994; Sjgren et al, 1996a).

Hair analysis is a poor indicator of aluminium exposure (Wilhelm et al, 1989). AT RISK GROUPS Preterm infants have a limited ability to excrete aluminium. OCCUPATIONAL DATA Occupational exposure standard Long term exposure limit (8 hour TWA reference period) total inhalable dust 10 mg/m 3, respirable dust 5mg/m 3 (Health and Safety Executive, 1995).

OTHER TOXICOLOGICAL DATA Carcinogenicity Workers involved in aluminium production may be at increased risk of developing lung cancer but mortality figures are difficult to interpret, especially when comprehensive occupational and smoking histories are not available (Andersen et al, 1982).

• Moreover, these workers are exposed to a number of established carcinogens including asbestos, chromium and polycyclic aromatic hydrocarbons (Dufresne et al, 1996).
• Higher than expected mortality from other cancers, including lymphoreticular and genitourinary malignancies have also been reported (Gibbs, 1981; Rockette and Arena, 1983) but again concomitant exposure to polycyclic aromatic hydrocarbons is likely to be involved (Thriault et al, 1984; Spinelli et al, 1991).

In 521 workers exposed to aluminium oxide in an abrasive manufacturing plant and followed up between 1958 and 1983 Edling et al (1987) found no significantly increased cancer morbidity or mortality. Reprotoxicity NIF Genotoxicity Bacillus subtilis H17 (rec + ), M45 (rec – ) negative DNA damage (DOSE, 1992).

• Fish toxicity NIF EEC Directive on Drinking Water Quality 80/778/EEC Aluminium: Guide level 0.05mg/L, maximum admissible concentration 0.2g/L (DOSE, 1992).
• WHO Guidelines for Drinking Water Quality No health-based guideline value is recommended (WHO,1993).
• AUTHORS SM Bradberry BSc MB MRCP ST Beer BSc JA Vale MD FRCP FRCPE FRCPG FFOM National Poisons Information Service (Birmingham Centre), West Midlands Poisons Unit, City Hospital NHS Trust, Dudley Road, Birmingham B18 7QH UK This monograph was produced by the staff of the Birmingham Centre of the National Poisons Information Service in the United Kingdom.

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Day JP, Ackrill P. The chemistry of desferrioxamine chelation for aluminum overload in renal dialysis patients. Ther Drug Monit 1993; 15: 598-601. Desjardins A, Bergeron JP, Ghezzo H, Cartier A, Malo JL. Aluminium potroom asthma confirmed by monitoring of forced expiratory volume in one second.

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Br J Ind Med 1991; 48: 735-8. Erasmus RT, Savory J, Wills MR, Herman MM. Aluminum neurotoxicity in experimental animals. Ther Drug Monit 1993; 15: 588-92. Exley C, Birchall JD. The cellular toxicity of aluminium. J Theor Biol 1992; 159: 83-98. Firling CE, Severson AR, Hill TA. Aluminum effects on blood chemistry and long bone development in the chick embryo.

Arch Toxicol 1994; 68: 541-7. Gibbs GW. Mortality experience in Eastern Canada. In: Hughes JP, ed. Health protection in primary aluminium production. Vol 2.2nd ed. London: London International Primary Aluminium Institute, 1981; 56-69. Gitelman HJ, Alderman FR, Kurs-Lasky M, Rockette HE.

• Serum and urinary aluminium levels of workers in the aluminium industry.
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Selective accumulation of aluminum and iron in the neurofibrillary tangles of Alzheimer’s disease: a laser microprobe (LAMMA) study. Ann Neurol 1992; 31: 286-92. Goodill JJ, Abuelo JG. Mucormycosis – a new risk of deferoxamine therapy in dialysis patients with aluminum or iron overload? N Engl J Med 1987; 31: 54.

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• Internal load of aluminum and the central nervous system function of aluminum welders.
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Haug A, Shi B, Vitorello V. Aluminum interaction with phosphoinositide-associated signal transduction. Arch Toxicol 1994; 68: 1-7. Health and Safety Executive. EH40/95. Occupational exposure limits 1995. Sudbury: Heath and Safety Executive, 1995. House RA. Factors affecting plasma aluminium concentrations in nonexposed workers.

J Occup Med 1992; 34: 1013-7. Jederlinic PJ, Abraham JL, Churg A, Himmelstein JS, Epler GR, Gaensler EA. Pulmonary fibrosis in aluminum oxide workers. Investigation of nine workers, with pathologic examination and microanalysis in three of them. Am Rev Respir Dis 1990; 142: 1179-84. Joshi JG, Dhar M, Clauberg M, Chauthaiwale V.

Iron and aluminum homeostasis in neural disorders. Environ Health Perspect 1994; 102: 207-13. Klatzo I, Wisniewski H, Streicher E. Experimental production of neurofibrillary degeneration.I. Light microscopic observations. J Neuropathol Exp Neurol 1965; 24: 187-99.

• Ongerud J, Gronnesby JK, Magnus P.
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Serial measurements of peak expiratory flow and responsiveness to methacholine in the diagnosis of aluminium potroom asthma. Thorax 1992; 47: 292-7. Kongerud J, Boe J, Syseth V, Naalsund A, Magnus P. Aluminium potroom asthma: the Norwegian experience. Eur Resp J 1994; 7: 165-72.

Kontoghiorghes GJ, Barr J, Baillod RA. Studies of aluminium, mobilization in renal dialysis patients using the oral chelator 1,2-dimethyl-3-hydroxypyrid-4-one. Arzneimittelforschung 1994; 44: 522-6. Kotovirta M-L, Salo OP, Visa-Tolvanen K. Contact sensitivity to aluminium. Contact Dermatitis 1984; 11: 135.

Ljunggren KG, Lidums V, Sjgren B. Blood and urine concentrations of aluminium among workers exposed to aluminium flake powders. Br J Ind Med 1991; 48: 106-9. Main J, Ward MK. Potentiation of aluminium absorption by effervescent analgesic tablets in a haemodialysis patient.

Br Med J 1992; 304: 1686. McCarthy JT, Milliner DS, Johnson WJ. Clinical experience with desferrioxamine in dialysis patients with aluminium toxicity. Q J Med 1990; 275: 257-76. McCauley J, Sorkin MI. Exacerbation of aluminium encephalopathy after treatment with desferrioxamine. Nephrol Dial Transplant 1989; 4: 110-4.

McLaughlin AIG, Kazantzis G, King E, Teare D, Porter RJ, Owen R. Pulmonary fibrosis and encephalopathy associated with the inhalation of aluminium dust. Br J Ind Med 1962; 19: 253-63. Mitchell J. Pulmonary fibrosis in an aluminium worker. Br J Ind Med 1959; 16: 123-5.

Mitchell J, Manning GB, Molyneux M, Lane RE. Pulmonary fibrosis in workers exposed to finely powdered aluminium. Br J Ind Med 1961; 18: 10-20. Munoz DG. Aluminum and Alzheimer’s disease. Can Med Assoc J 1994; 151: 268. Murray JC, Tanner CM, Sprague SM. Aluminum neurotoxicity: a re-evaluation. Clin Neuropharmacol 1991; 14: 179-85.

Nielsen J, Dahlqvist M, Welinder H, Thomassen Y, Alexandersson R, Skerfving S. Small airways function in aluminium and stainless steel welders. Int Arch Occup Environ Health 1993; 65: 101-5. O’Brien AA, McParland C, Keogh JA. The use of intravenous and intraperitoneal desferrioxamine in aluminium osteomalacia.

Nephrol Dial Transplant 1987; 2: 117-9. Petit TL. Issues in aluminum neurotoxicology. Comments Toxicol 1989; 3: 225-38. Pierre F, Baruthio F, Diebold F, Biette P. Effect of different exposure compounds on urinary kinetics of aluminium and fluoride in industrially exposed workers. Occup Environ Med 1995; 52: 396-403.

Rifat SL, Eastwood MR, Crapper McLachlan DR, Corey PN. Effect of exposure of miners to aluminium powder. Lancet 1990; 336: 1162-5. Rockette HE, Arena VC. Mortality studies of aluminum reduction plant workers: potroom and carbon department. J Occup Med 1983; 25: 549-57.

Rllin HB, Theodorou P, Kilroe-Smith TA. The effect of exposure to aluminium on concentrations of essential metals in serum of foundry workers. Br J Ind Med 1991; 48: 243-6. Rllin HB, Theodorou P, Cantrell AC. Biological indicators of exposure to total and respirable aluminium dust fractions in a primary aluminium smelter.

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Eosinophilic lung reaction to aluminium and hard metal. Chest 1994; 105: 1261-3. Sjgren B, Gustavsson P, Hogstedt C. Neuropsychiatric symptoms among welders exposed to neurotoxic metals. Br J Ind Med 1990; 47: 704-7. Sjgren B, Ljunggren KG, Almkvist O, Frech W, Basun H.

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Is ammonium hydroxide bad for skin?

Contact can severely irritate and burn the skin and eyes leading to eye damage. ► Exposure can irritate the eyes, nose and throat. ► Inhaling Ammonium Hydroxide can irritate the lungs. Higher exposures may cause a build-up of fluid in the lungs (pulmonary edema), a medical emergency.

Is aluminium toxic to skin?

If you’re a clean beauty junkie, chances are you’ve heard about the negative effects aluminum can have in your products. For years now, babes everywhere have been concerned about the toxicity that is found in this questionable ingredient. What’s more, research has shown that harmful short and long-term effects are associated with the use of aluminum in topically applied products. We’re not talking about the aluminum foil you wrap up those leftovers in, babe. Nope – aluminum goes way beyond your bottom drawer in the kitchen. And honestly, we really wish it didn’t. For the sake of this blog post though, we’re referring to the aluminum that is often found in antiperspirants.

1. You know, the one they use to help you sweat less by clogging your pores.
2. Umm, talk about an undesirable outcome.
3. I mean, you might want to sweat less during that wicked Peloton session, but is it really worth clogging your pores over? We didn’t think so, either.
4. Beyond the pore-blocking fiasco, we should also mention that aluminum is a common element that can be found all around us.

And even though it is popularly known as a culprit in antiperspirant, it can actually be found in a variety of everyday items. From toothpaste to food additives, this is one ingredient you’ll be annoyed to know can creep up almost anywhere. Yeah, now might be a good time to start using less of that foil #amirite? Not to get too technical on you, but aluminum can come in the form of what are called “compounds”.

1. This means that this element is often paired off with other active ingredients in your products.
2. For example, if you use traditional antiperspirant, we bet that you’ll find something along the lines of “aluminum zirconium tetrachlorohydrex GLY” on the back of it.
3. We know, it’s a mouthful.
4. And on top of that, it’s totally unnecessary to keeping you smelling fresh all day long.

But we’ll get into that a little later, so stay tuned gorgeous. Those who are adamantly against the use of aluminum claim that preventing perspiration can mean that you are not sweating out cancer-causing toxins. However, more research is needed on to confirm this and your kidneys and liver are actually what eliminates these unwanted toxins from your body.

Despite these facts, some research has shown that the use of aluminum in large amounts can indeed be harmful. Experts have uncovered that exposing yourself to too much aluminum can cause hormone imbalances which in turn affects your overall health. We covered the many dangers of hormone imbalances in our blog post on parabens, so if you want to brush up on what some of those effects are – click here, babe.

Now if you’re wondering about short-term side effects of aluminum use, here’s what you need to know. Skin issues from acne to dry irritation can all be not so cute results from using this undesirable ingredient. This doesn’t mean every babe will experience these issues, however if you find yourself with itchy armpits after applying that antiperspirant – it could definitely be due to the aluminum in it. Here’s how the aluminum cookie crumbles, babe. Alright that sounds gross, but you get where we’re going with this. Even though further evidence is needed to solidify the notion that aluminum use can lead to more serious long-term health effects such as cancer and other diseases like Alzheimer’s, the truth is this.

1. There is no reason to even risk these types of terrible side effects when there are natural alternatives out there that quite honestly, work even better than those aluminum-infused nasties.
2. So if you think you have to apply aluminum-packed products to smell fresh as a daisy, think again.
3. There is a *ton* of natural alternatives to the everyday products you might be using right now.

Just stick with this post on the Danger of Aluminum Ingredients in Skincare Products to discover them, gorgeous. As we noted at the begging of this blog on the Danger of Aluminum Ingredients in Skincare Products, this element is mostly known for its role in antiperspirant.

It is typically not found in deodorants, because these guys do not cause you to not sweat. Instead, deodorant just neutralizes any unwanted smells which honestly – we totally appreciate. As we’ve briefly mentioned, you should also know that aluminum derivatives can be found in cosmetics. We’re talking lipstick, blush, and almost any other product you use on the regular to get glammed up.

Tragic, we know. The reason companies include this nasty ingredient in makeup can range from preventing color bleeding to using it as a thickening agent, Luckily though, so many brands have jumped on the natural bandwagon in favor of ditching this nasty ingredient.

• This means that finding safe alternatives to your go-to makeup items is *way* easier than it once was.
• If at this point you’re ready to give your makeup bag a complete revamp, we feel that.
• Start your cosmetic spring cleaning off right and check out this list of EWG approved brands that prioritize safe ingredients.

And hey, who wouldn’t love curating a new clean cosmetic collection? We’ve got you, babe. Babe, now comes our favorite part of this whole post on the Danger of Aluminum Ingredients in Skincare Products. Let’s just say, avoiding aluminum in your favorite beauty and skincare items is just as easy as muting your ex’ IG story.

1. Check this out.
2. The skincare and beauty suggestions we have under our belt will only make you wonder why you didn’t make the switch to safer products sooner! Clean, effective, and a breeze to use: here are what we consider aluminum-free must-haves that you should click add to cart on, right now.
3. BBE’s aluminum-free deodorant Aluminum, who? With powerful yet safe magnesium alone, you (and your armpits) can happily say adios to that pore-clogging ingredient.

Magnesium on the other hand combats funk without ever blocking your precious pores. We made this bad boy in a variety of scents every babe can fall in love with. From lavender to vanilla coconut, you’ll be smelling like a dream sans harsh side effects. BBE’s tinted sunscreens Did you know that so many makeup brands use aluminum in their foundation formulas? It’s the #truth babe. Applying a bit of liquid gold to your face everyday might seem harmless, but in the long run you already know what the risks are. BBE’s moisturizing lippies Lipstick is yet another makeup item that is packed with aluminum to enrich its color. And while we know how tempting it can be to sport the perfect-colored pout, the negative side effects just aren’t worth it in our books. Instead, opt for a nourishing lip balm from BBE that will bring out the natural color of your lips. And now, so are you! I mean, now that you know all about the danger of aluminum ingredients in skincare products, how could you not be ready to move on to bigger, better, and safer things? And with all the unreal beauty and skincare alternatives out there, you can get excited about ditching aluminum once and for all. Finally babe, we cannot say this enough. You don’t have to compromise your health for the sake of anything beauty related – aluminum included. That’s our promise to you and the reason why we are so obsessively natural. If you’ve made the switch to aluminum-free products, we want to hear all about your journey below. And if you need more tips on how to make the transition, drop us a line any time. Love & (aluminum-free) Lip Balm, Carey <3