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Cancer risk after acetaldehyde and formaldehyde indoor exposure
50 ASSESSMENT
Pharmacological Research, kbl. 26, Supplement I, 1992 OF THE POSSIBLE
D. F. Weetman Schoo 1 of Health Sciences, SRl 350, England Sunderland,
RISK
TO HEALTH
University
FROM BUILDINGS.
of
Sunderland,
A distinction should be made between building-related diseases and intolerance to buildings (sick building Substances are most likely to exert an effect syndrome). via the lungs or by acting topically. A paradigm is proposed for the evaluation of possible health effects from Hypothesis-generating information indoor air pollutants. occupational medicine, epidemiology, comes from experimental pathology and animal toxicology. The testing multi-factorial of hypotheses is complicated by the aetiology of many diseases, the difficulty in evaluating the effects of mixtures, and in extrapolation of dose. The of reactive population at risk may contain sub-groups Although association between a pollutant and individuals. causation is rarely established an effect may be apparent, Indoor air hazards include in the non-industrial setting. origin, microbes, allogens of microbial pathogenic particles and fibres, aerosols, radon and its relatives, polyaromatic hydrocarbons and various gaseous oxides.
CANCER RISK AFTER ACETALDEHYDE AND FORMALDEHYDE INDOOR EXPOSURE. Mario Mangrella, Maria Luigia Cenicola, Enrico Lampa and Francesco Rossi Institute of Pharmacology and Toxicology, 1st Faculty of Medicine and Surgery, University of Naples Federico II, Naples, Italy Many substances are capable of causing genetic damage. During the everyday life, cells constantly suffer damages to their nuclear DNA. If the repair defenses fail, the impact of the damage on the physiological activities of some tissues is minimized by the rapid cell turnover (epidermis, bone marrow, gut lining, etc.), or by the immune defense. The genotoxicity of the inhaled acetaldehyde and particularly formaldehyde is well known. However, these products are responsible for more other effects on the different areas of the respiratory tract, such as severe inflammation, hyperplasia, metaplasia, etc. A lot of sources of acetaldehyde and formaldehyde exposure actually exists, e.g. residential wood combustion, coffee roasting, acetic acid, vinyl acetate, ethanol and acrylonitrile manufacturers, embalming, resin manufacture and paper production, textile products, homes constructed with particle board, mobile homes, etc. Moreover, acetaldehyde is the first product of ethanol oxidation in the liver. Epidemiologic studies concluded that the exposure to low concentrations of acetaldehyde and formaldehyde present in air may be responsible for a cancer risk. However, laboratory results suggest that this risk increases with the chronic exposure to high concentrations. It seems that acetaldehyde and formaldehyde act by an irritation associated with a stimulation of the cellular proliferation. However, in humans only the exposure to concentrations that led to severe irritation of the nasal epithelium with reparative hyperplasia may represent a risk of developing nasal cancer. In particular, the carcinogenicity of high concentrations of these compounds results from a combination of weak tumour initiating genotoxicity and tumour promoting activity associatedwith mucosal cytotoxicity and other tissutal lesions.
Pharmacological Research, kbl. 26, Supplement I, 1992 OF THE POSSIBLE
D. F. Weetman Schoo 1 of Health Sciences, SRl 350, England Sunderland,
RISK
TO HEALTH
University
FROM BUILDINGS.
of
Sunderland,
A distinction should be made between building-related diseases and intolerance to buildings (sick building Substances are most likely to exert an effect syndrome). via the lungs or by acting topically. A paradigm is proposed for the evaluation of possible health effects from Hypothesis-generating information indoor air pollutants. occupational medicine, epidemiology, comes from experimental pathology and animal toxicology. The testing multi-factorial of hypotheses is complicated by the aetiology of many diseases, the difficulty in evaluating the effects of mixtures, and in extrapolation of dose. The of reactive population at risk may contain sub-groups Although association between a pollutant and individuals. causation is rarely established an effect may be apparent, Indoor air hazards include in the non-industrial setting. origin, microbes, allogens of microbial pathogenic particles and fibres, aerosols, radon and its relatives, polyaromatic hydrocarbons and various gaseous oxides.
CANCER RISK AFTER ACETALDEHYDE AND FORMALDEHYDE INDOOR EXPOSURE. Mario Mangrella, Maria Luigia Cenicola, Enrico Lampa and Francesco Rossi Institute of Pharmacology and Toxicology, 1st Faculty of Medicine and Surgery, University of Naples Federico II, Naples, Italy Many substances are capable of causing genetic damage. During the everyday life, cells constantly suffer damages to their nuclear DNA. If the repair defenses fail, the impact of the damage on the physiological activities of some tissues is minimized by the rapid cell turnover (epidermis, bone marrow, gut lining, etc.), or by the immune defense. The genotoxicity of the inhaled acetaldehyde and particularly formaldehyde is well known. However, these products are responsible for more other effects on the different areas of the respiratory tract, such as severe inflammation, hyperplasia, metaplasia, etc. A lot of sources of acetaldehyde and formaldehyde exposure actually exists, e.g. residential wood combustion, coffee roasting, acetic acid, vinyl acetate, ethanol and acrylonitrile manufacturers, embalming, resin manufacture and paper production, textile products, homes constructed with particle board, mobile homes, etc. Moreover, acetaldehyde is the first product of ethanol oxidation in the liver. Epidemiologic studies concluded that the exposure to low concentrations of acetaldehyde and formaldehyde present in air may be responsible for a cancer risk. However, laboratory results suggest that this risk increases with the chronic exposure to high concentrations. It seems that acetaldehyde and formaldehyde act by an irritation associated with a stimulation of the cellular proliferation. However, in humans only the exposure to concentrations that led to severe irritation of the nasal epithelium with reparative hyperplasia may represent a risk of developing nasal cancer. In particular, the carcinogenicity of high concentrations of these compounds results from a combination of weak tumour initiating genotoxicity and tumour promoting activity associatedwith mucosal cytotoxicity and other tissutal lesions.