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Recent trend in risk assessment of formaldehyde exposures from indoor air.

ABSTRACT: Studies about formaldehyde (FA) published since the guideline of 0.1 mg/m(3) by the World Health Organization (WHO) in 2010 have been evaluated; critical effects were eye and nasal (portal-of-entry) irritation. Also, it was considered to prevent long-term effects, including all types of cancer. The majority of the recent toxicokinetic studies showed no exposure-dependent FA-DNA adducts outside the portal-of-entry area and FA-DNA adducts at distant sites were due to endogenously generated FA. The no-observed-adverse-effect level for sensory irritation was 0.5 ppm and recently reconfirmed in hypo- and hypersensitive individuals. Investigation of the relationship between FA exposure and asthma or other airway effects in children showed no convincing association. In rats, repeated exposures showed no point mutation in the p53 and K-Ras genes at ?15 ppm neither increased cell proliferation, histopathological changes and changes in gene expression at 0.7 ppm. Repeated controlled exposures (0.5 ppm with peaks at 1 ppm) did not increase micronucleus formation in human buccal cells or nasal tissue (0.7 ppm) or in vivo genotoxicity in peripheral blood lymphocytes (0.7 ppm), but higher occupational exposures were associated with genotoxicity in buccal cells and cultivated peripheral blood lymphocytes. It is still valid that exposures not inducing nasal squamous cell carcinoma in rats will not induce nasopharyngeal cancer or lymphohematopoietic malignancies in humans. Reproductive and developmental toxicity are not considered relevant in the absence of sensory irritation. In conclusion, the WHO guideline has been strengthened.

SUBMITTER: Nielsen GD

PROVIDER: S-EPMC3618407 | biostudies-literature | 2013 Jan

REPOSITORIES: biostudies-literature

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Recent trend in risk assessment of formaldehyde exposures from indoor air.

Nielsen Gunnar Damgård GD Larsen Søren Thor ST Wolkoff Peder P

Archives of toxicology 20121121 1

Studies about formaldehyde (FA) published since the guideline of 0.1 mg/m(3) by the World Health Organization (WHO) in 2010 have been evaluated; critical effects were eye and nasal (portal-of-entry) irritation. Also, it was considered to prevent long-term effects, including all types of cancer. The majority of the recent toxicokinetic studies showed no exposure-dependent FA-DNA adducts outside the portal-of-entry area and FA-DNA adducts at distant sites were due to endogenously generated FA. The ...[more]

PMID: 23179754

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Project description:IntroductionDirect emissions of nicotine and harmful chemicals from electronic cigarettes (e-cigarettes) have been intensively studied, but secondhand and thirdhand e-cigarette aerosol (THA) exposures in indoor environments are understudied.Aims and methodsIndoor CO2, NO2, particulate matter (PM2.5), aldehydes, and airborne nicotine were measured in five vape-shops to assess secondhand exposures. Nicotine and tobacco-specific nitrosamines were measured on vape-shop surfaces and materials (glass, paper, clothing, rubber, and fur ball) placed in the vape-shops (14 days) to study thirdhand exposures.ResultsAirborne PM2.5, formaldehyde, acetaldehyde, and nicotine concentrations during shop opening hours were 21, 3.3, 4.0, and 3.8 times higher than the levels during shop closing hours, respectively. PM2.5 concentrations were correlated with the number of e-cigarette users present in vape-shops (ρ = 0.366-0.761, p < .001). Surface nicotine, 4-(N-methyl-N-nitrosamino)-4-(3-pyridyl)butanal (NNA), and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) were also detected at levels of 223.6 ± 313.2 µg/m2, 4.78 ± 11.8 ng/m2, and 44.8 ± 102.3 ng/m2, respectively. Substantial amounts of nicotine (up to 2073 µg/m2) deposited on the materials placed within the vape-shops, and NNA (up to 474.4 ng/m2) and NNK (up to 184.0 ng/m2) were also formed on these materials. The deposited nicotine concentrations were strongly correlated with the median number of active vapers present in a vape-shop per hour (ρ = 0.894-0.949, p = .04-.051). NNK levels on the material surfaces were significantly associated with surface nicotine levels (ρ=0.645, p = .037).ConclusionsIndoor vaping leads to secondhand and THA exposures. Thirdhand exposures induced by e-cigarette vaping are comparable or higher than that induced by cigarette smoking. Long-term studies in various microenvironments are needed to improve our understanding of secondhand and THA exposures.ImplicationsThis study adds new convincing evidence that e-cigarette vaping can cause secondhand and THA exposures. Our findings can inform Occupational Safety and Health Administration, state authorities, and other government agencies regarding indoor air policies related to e-cigarette use, particularly in vape-shops. There is an urgent need to ensure that vape-shops maintain suitable ventilation systems and cleaning practices to protect customers, employees, and bystanders. Our study also demonstrates that nicotine can deposit or be adsorbed on baby's clothes and toys, and that tobacco-specific nitrosamines can form and retain on baby's clothes, highlighting children's exposure to environmental e-cigarette aerosol and THA at home is of a particular concern.

Project description:Few epidemiologic studies have evaluated the effects of air pollution on the risk of Parkinson disease (PD).We investigated the associations of long-term residential concentrations of ambient particulate matter (PM) < 10 ?m in diameter (PM10) and < 2.5 ?m in diameter (PM2.5) and nitrogen dioxide (NO2) in relation to PD risk.Our nested case-control analysis included 1,556 self-reported physician-diagnosed PD cases identified between 1995 and 2006 and 3,313 controls frequency-matched on age, sex, and race. We geocoded home addresses reported in 1995-1996 and estimated the average ambient concentrations of PM10, PM2.5, and NO2 using a national fine-scale geostatistical model incorporating roadway information and other geographic covariates. Air pollutant exposures were analyzed as both quintiles and continuous variables, adjusting for matching variables and potential confounders.We observed no statistically significant overall association between PM or NO2 exposures and PD risk. However, in preplanned subgroup analyses, a higher risk of PD was associated with higher exposure to PM10 (ORQ5 vs. Q1 = 1.65; 95% CI: 1.11, 2.45; p-trend = 0.02) among women, and with higher exposure to PM2.5 (ORQ5 vs. Q1 = 1.29; 95% CI: 0.94, 1.76; p-trend = 0.04) among never smokers. In post hoc analyses among female never smokers, both PM2.5 (ORQ5 vs. Q1 = 1.79; 95% CI: 1.01, 3.17; p-trend = 0.05) and PM10 (ORQ5 vs. Q1 = 2.34; 95% CI: 1.29, 4.26; p-trend = 0.01) showed positive associations with PD risk. Analyses based on continuous exposure variables generally showed similar but nonsignificant associations.Overall, we found limited evidence for an association between exposures to ambient PM10, PM2.5, or NO2 and PD risk. The suggestive evidence that exposures to PM2.5 and PM10 may increase PD risk among female never smokers warrants further investigation. Citation: Liu R, Young MT, Chen JC, Kaufman JD, Chen H. 2016. Ambient air pollution exposures and risk of Parkinson disease. Environ Health Perspect 124:1759-1765;?http://dx.doi.org/10.1289/EHP135.

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Recent trend in risk assessment of formaldehyde exposures from indoor air.

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Recent trend in risk assessment of formaldehyde exposures from indoor air.

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