Abstract

Air pollution has been recognized as a human carcinogen. Children living in urban areas are a high-risk group, because genetic damage occurring early in life is considered able to increase the risk of carcinogenesis in adulthood. This study aimed to investigate micronuclei (MN) frequency, as a biomarker of DNA damage, in exfoliated buccal cells of pre-school children living in a town with high levels of air pollution. A sample of healthy 3-6-year-old children living in Brescia, Northern Italy, was investigated. A sample of the children’s buccal mucosa cells was collected during the winter months in 2012 and 2013. DNA damage was investigated using the MN test. Children’s exposure to urban air pollution was evaluated by means of a questionnaire filled in by their parents that included items on various possible sources of indoor and outdoor pollution, and the concentration of fine particulate matter (PM10, PM2.5) and NO2 in the 1–3 weeks preceding biological sample collection. 181 children (mean age±SD: 4.3±0.9 years) were investigated. The mean±SD MN frequency was 0.29±0.13%. A weak, though statistically significant, association of MN with concentration of air pollutants (PM10, PM2.5 and NO2) was found, whereas no association was apparent between MN frequency and the indoor and outdoor exposure variables investigated via the questionnaire. This study showed a high MN frequency in children living in a town with heavy air pollution in winter, higher than usually found among children living in areas with low or medium-high levels of air pollution.

Abstract

Background

Although the International Agency for Research on Cancer (IARC) has classified various indoor air pollutants as carcinogenic to humans, few studies evaluated the role of household ventilation in reducing the impact of indoor air pollutants on lung cancer risk.

Objectives

To explore the association between household ventilation and lung cancer.

Methods

A population-based case-control study was conducted in a Chinese population from 2003 to 2010. Epidemiologic and household ventilation data were collected using a standardized questionnaire. Unconditional logistic regression was employed to estimate adjusted odds ratios (ORadj) and their 95% confidence intervals (CI).

Results

Among 1,424 lung cancer cases and 4,543 healthy controls, inverse associations were observed for good ventilation in the kitchen (ORadj = 0.86, 95% CI: 0.75, 0.98), bedroom (ORadj= 0.90, 95% CI: 0.79, 1.03), and both kitchen and bedroom (ORadj = 0.87, 95% CI: 0.75, 1.00). Stratified analyses showed lung cancer inversely associated with good ventilation among active smokers (ORadj = 0.85, 95% CI: 0.72, 1.00), secondhand smokers at home (ORadj = 0.77, 95% CI: 0.63, 0.94), and those exposed to high-temperature cooking oil fumes (ORadj = 0.82, 95% CI: 0.68, 0.99). Additive interactions were found between household ventilation and secondhand smoke at home as well as number of household pollutant sources.

Conclusions

A protective association was observed between good ventilation of households and lung cancer, most likely through the reduction of exposure to indoor air pollutants, indicating ventilation may serve as one of the preventive measures for lung cancer, in addition to tobacco cessation.

Abstract

Background

The air pollution caused by vehicular emissions is associated with cognitive decline. However, the associations between the levels of nitrogen dioxide (NO2) and carbon monoxide (CO) exposure and dementia remain poorly defined and have been addressed in only a few previous studies.

Materials and Methods

In this study, we obtained data on 29547 people from the National Health Insurance Research Database (NHIRD) of Taiwan, including data on 1720 patients diagnosed with dementia between 2000 and 2010, and we evaluated the risk of dementia among four levels of air pollutant. Detailed data on daily air pollution were available from January 1, 1998 to December 31, 2010. Yearly average concentrations of pollutants were calculated from the baseline to the date of dementia occurrence, withdrawal of patients, or the end of the study, and these data were categorized into quartiles, with Q1 being the lowest level and Q4 being the highest.

Results

In the case of NO2, the adjusted hazard ratios (HRs) of dementia for all participants in Q2, Q3, and Q4 compared to Q1 were 1.10 (95% confidence interval (CI), 0.96–1.26), 1.01 (95% CI, 0.87–1.17), and 1.54 (95% CI, 1.34–1.77), and in the case of CO, the adjusted HRs were 1.07 (95% CI, 0.92–1.25), 1.37 (95% CI, 1.19–1.58), and 1.61 (95% CI, 1.39–1.85).

Conclusion

The results of this large retrospective, population-based study indicate that exposure to NO2and CO is associated with an increased risk of dementia in the Taiwanese population.

Abstract

Background

Criteria pollutants have been associated with exacerbation of children’s asthma, but the role of air toxics in relation to asthma is less clear. Our objective was to evaluate whether exposure to outdoor air toxics in early childhood increased asthma risk or severity.

Methods

Air toxics exposure was estimated using the 2002 National Air toxics Assessment (NATA) and linked to longitudinal data (n=6950) from a representative sample of US children born in 2001 and followed through kindergarten-age in the Early Child Longitudinal Study – Birth Cohort (ECLS-B).

Results

Overall, 17.7% of 5.5 year-olds had ever been told by a healthcare professional they had asthma, and 6.8% had been hospitalized or visited an emergency room for an asthma attack. Higher rates of asthma were observed among boys (20.1%), low-income (24.8%), and non-Hispanic black children (30.0%) (p≤0.05). Air toxics exposure was greater for minority race/ethnicity (p<0.0001), low income (p<0.0001), non-rural area (p<0.001). Across all analyses, greater air toxics exposure, as represented by total NATA respiratory hazard index, or when limited to respiratory hazard index from onroad mobile sources or diesel PM, was not associated with a greater prevalence of asthma or hospitalizations (p trend >0.05). In adjusted logistic regression models, children exposed to the highest respiratory hazard index were not more likely to have asthma compared to those exposed to the lowest respiratory hazard index of total, onroad sources, or diesel PM.

Conclusions

Early childhood exposure to outdoor air toxics in a national sample has not previously been studied relative to children’s asthma. Within the constraints of the study, we found no evidence that early childhood exposure to outdoor air toxics increased risk for asthma. As has been previously reported, it is evident that there are environmental justice and disparity concerns for exposure to air toxics and asthma prevalence in US children.