Tobacco smoke exposes children to lead

Researchers at the Hopkins Bloomberg School of Public Health have found that children in the Unites States exposed to secondhand tobacco smoke show an increase in blood lead levels. This is an additional hazard of tobacco smoke, which is already acknowledged widely as a major source of indoor air pollution. Exposure to secondhand smoke is responsible for several health problems in children including lower respiratory tract infections and reduced lung growth.

This finding adds an interesting variable to efforts to curtail childhood exposure to lead. Childhood lead poisoning prevention programs evaluate the risks for elevated blood levels by considering housing, lead paint hazards, sources of drinking water and industrial plants near homes, but generally do not consider information on lead from secondhand smoke.

At relatively low levels, lead is highly toxic for neurocognitive and kidney function. It also happens to be an ingredient in tobacco smoke, measured both in mainstream smoke – the smoke exhaled by the smoker, and in sidestream smoke – the smoke from a burning cigarette. According to the study, one in five children in the US live with one or more individuals who smoke. Globally, this figure is even higher. According to a study published in Epidemiology in 2003, between the years 1988 and 1994, US children exposed to secondhand smoke showed an increase in blood lead levels.

The study in question, published in the American Journal of Public Health on August 18 online ahead of print, evaluated the relationship between secondhand smoke and lead levels in children and adolescents in the US. The researchers analyzed data from participants between the ages of 3 and 19 in the National Health and Nutrition Examination Survey (NHANES), conducted between 1999 and 2004. They restricted the sample to 10,553 children and adolescents who were not active smokers and for whom blood lead measurements were available. Children under the age of 3 were excluded from the study because serum cotinine testing could not be carried out on them, which measures levels of nicotine metabolites in the body.

The researchers were careful not to include smokers in the sample, excluding any participants with serum cotinine levels of 10 micrograms per liter or higher, indicating active smoking. The final number of participants in the study was 6,830. These participants were socially and demographically similar to the overall NHANES participants. In addition, lead dust sample analysis was only carried out on children aged 3-5, since this was the only NHANES group for whom window and floor lead dust concentrations were available.

The secondhand smoke exposure was assessed using self-reported data and serum cotinine levels, measured by the National Center for Environmental Health, Centers for Disease Control and Prevention (CDC) by means of high performance liquid chromatography/mass spectrometry. The limit of detection was 0.05 micrograms per liter for the first phase of NHANES (1999-2000) and 0.15 micrograms for the second and third phases (2001-2002, 2003-2004). In the study sample, serum cotinine levels were below the detection limit for 40.1% of participants in NHANES (1999-2000), 23.4% in NHANES (2001-2002), and 16.4% of participants in NHANES (2003-2004). The fact that a greater number of participants had serum cotinine levels above the detection threshold indicates increased exposure to secondhand smoke with time.

Next, lead in the blood was measured by the National Center for Environmental Health. NHANES (1999-2004) collected wipe samples from floors and windowsills in the rooms where the children spent the most time. The lead content of these samples was also measured.

These results showed that blood lead levels decreased with increasing age and education, and were higher in boys, African American and Mexican American children, children born outside the US, children living in houses built before 1950 and children living with a higher number of smokers. Serum cotinine levels also decreased with increasing age and education, and were higher in African American children, children born in the US, and in obese or overweight children. Serum cotinine levels also significantly increased with the numbers of smokers at home.

Researchers found that living with one or more smokers and increasing serum cotinine levels were connected to higher blood lead levels in non-smoking children and adolescents from NHANES. Blood lead levels increased steadily with secondhand smoke; this correlation was even greater in younger children, perhaps due to a greater amount of time spent at home or with their parents and family members compared to older children.

The study supports the suggestion that secondhand smoke contributes to elevated blood levels, and is a preventable source of lead exposure in US children. The authors of the study suggest that lead prevention programs should systematically evaluate smoking at home and provide smoke-free environments for children to reduce lead exposure. Measures to eliminate secondhand smoke exposure in children could contribute to lower blood lead levels, and possibly a decrease in lead-related detrimental health effects.