Objectives. This study examined the effect of an active program of household lead paint hazard abatement, applied over 22 years, on childhood lead poisoning in Massachusetts. Methods. A small areas analysis was used to compare screening blood lead levels of children in Worcester County, Mass (n = 27590), with those in Providence County, RT (n = 19071). Data were collapsed according to census tract. Results. The percentage of children with lead poisoning (blood lead level greater than or equal to 20 mu g/dL [Pe20]) was, on average, 3 times higher in Providence County census tracts (3.2% vs 0.9% in Worcester County census tracts, P < .0001), despite similar percentages of pre-1950s housing in both counties. The ratio of Pe20 in Providence vs Worcester County census tracts was 2.2 (95% confidence interval = 1.8. 2.7), after adjustment for differences in housing, sociodemographic, and screening characteristics. This estimate was robust to alternative regression methods and sensitivity analyses. Conclusions. Massachusetts policy, which requires lead paint abatement of children's homes and places liability for lead paint poisoning on property owners, may have substantially reduced childhood lead poisoning in that state.

OBJECTIVE. The objective of this study was to measure the effectiveness of intensive case management to reduce blood lead levels (BLLs) in children. Lead poisoning remains a common, preventable pediatric condition despite advances in reducing children's BLLs in the United States. Substantial evidence implicates lead paint–contaminated house dust as the most common high-dose source of lead in children's environments. Housekeeping and parental supervision also may contribute to risk for lead exposure.METHODS. We conducted a community-based, randomized trial of comprehensive education and home visiting for families of children with BLLs 15 to 19 μg/dL. BLLs after 1 year of follow-up were compared for intervention group children, whose families received individualized education that was designed to address specific risks factors in a child's environment, and comparison group children, whose families received customary care, usually 1 or 2 educational visits. Environmental samples were collected at baseline and after 1 year of follow-up for intervention group children and compared with those of comparison group children, collected only at the end of study.RESULTS. During the follow-up period, parents of intervention group children (n = 92) successfully decreased dust lead levels and significantly improved parent-child interaction and family housekeeping practices compared with comparison group children (n = 83). Overall geometric mean BLLs declined by 47%, and the difference in BLL by group was not significant (9 vs 8.3 μg/dL for intervention versus comparison group children, respectively.) After 1 year, nearly half of enrolled children had BLLs ≥10 μg/dL.CONCLUSIONS. Until a reservoir of lead-safe housing is created, programs that educate families to reduce environmental exposure are needed. Although providing families with quantitative information regarding lead contamination may have a role in short-term efforts to prevent lead exposure, these null findings suggest that it has little benefit once BLLs are elevated.

Exposure of children to ionizing radiation most commonly is from the environment, chiefly through cosmic rays and radon, or from medical technology. Medical radiation exposure occurs during diagnosis, therapy, and dental radiography. More is known about the biological effects of exposure to ionizing radiation than to nonionizing radiation from microwaves, radiowaves, and the electrical fields of other electrical appliances. This review applies only to sources of ionizing radiation and does not include the potential risks of indoor radon. The effects on children of ionizing radiation have been studied from war activities and environmental accidents. Projections are made from that data to help pediatricians evaluate risk from radiation when ordering radiographs.

Results of epidemiologic studies provide strong evidence that exposure of children to environmental tobacco smoke is associated with increased rates of lower respiratory illness and increased rates of middle ear effusion, asthma, and sudden infant death syndrome. Exposure during childhood may also be associated with development of cancer during adulthood. This statement reviews the health effects of environmental tobacco smoke on children and offers pediatricians a strategy for promoting a smoke-free environment. EFFECTS OF TOBACCO SMOKE ON CHILDREN In 1992, 48 million American adults (26.5%) currently smoked cigarettes.1 A recent national survey indicated that 43% of children 2 months to 11 years of age live in homes with at least one smoker.2 Because many young children spend a large proportion of their time indoors,3 they may have significant exposure to environmental tobacco smoke. Environmental tobacco smoke from cigarettes, cigars, and pipes is composed of more than 3800 different chemical compounds.4 Concentrations of respirable suspended particulate matter (particulates of ,2.5 mm) can be two to three times higher in homes with smokers than in homes with no smokers.5 Cigarette smoking is the most important factor determining the level of suspended particulate matter and respirable sulfates and particles in indoor air.6,7 Passive smoking has a harmful effect on the respiratory health of children.4,8,9 This statement reviews the evidence that children exposed to environmental tobacco smoke have higher rates of lower respiratory illness during their first year of life, higher rates of middle ear effusion, and higher rates of sudden infant death syndrome. In addition, children with asthma whose parents smoke have more severe symptoms and more frequent exacerbations. Passive Smoking and Lower Respiratory Illness The first effect of passive smoking to be documented in children was an increased rate of illnesses affecting the lower respiratory tract. Cameron10 reported a positive correlation between the presence of a smoker in the home and the incidence of perceived disease in children. Harlap and Davies11 interviewed pregnant women to determine their smoking habits and then studied hospital admissions for infants younger than 1 year. The infants whose mothers smoked were 38% more likely to be admitted to the hospital for bronchitis and pneumonia than were those whose mothers did not smoke. This increased likelihood was mainly among infants 6 to 9 months of age; admissions increased with the number of cigarettes smoked by the infants’ mothers. Rantakallio12 showed that, among children younger than 1 year, those with mothers who smoked cigarettes were almost four times as likely to be hospitalized as were the infants of nonsmoking mothers, and the number of hospitalizations increased with the number of cigarettes the mother smoked per day. During the first 5 years of life, pneumonia and bronchitis were about twice as likely and acute nasopharyngitis and sinusitis in the upper respiratory tract were about 1.5 times as likely to develop in children whose mothers smoke. Colley et al13 found a consistent gradient in the incidence of pneumonia and bronchitis in the child’s first year of life in relation to the parents’ smoking habits. Infants with two parents who smoked were more than twice as likely to have had pneumonia and bronchitis as were infants with parents who did not smoke. Fergusson et al14 showed that pneumonia and bronchitis in an infant’s first year of life increased with increasing maternal smoking in an approximately linear manner: increases of five cigarettes a day resulted in an increase of 2.5 to 3.5 incidents of lower respiratory illness per 100 children at risk. Passive Smoking and Serious Infectious Illnesses Berg and colleagues15 determined that among children 3 to 59 months of age, passive smoking was associated with an almost fourfold risk of a serious infectious illness requiring hospitalization. Passive Smoking and Middle Ear Effusions After a case-control study of risk factors for persistent middle ear effusions in Seattle, Kraemer and colleagues16 reported that children who lived in households where more than three packs of cigarettes were smoked per day were more than four times as likely to be admitted to the hospital for tympanostomy tube placement than were children whose parents did not smoke. Iversen and colleagues17 studied children up to 7 years of age in Danish day care centers and demonstrated that middle ear effusion as measured by tympanometry was about 60% more likely to develop in children whose parents smoked. They estimated the overall fraction of middle ear effusion attributable to passive smoking to be 15%. The recommendations in this statement do not indicate an exclusive course of treatment or serve as a standard of medical care. Variations, taking into account individual circumstances, may be appropriate. PEDIATRICS (ISSN 0031 4005). Copyright © 1997 by the American Academy of Pediatrics. PEDIATRICS Vol. 99 No. 4 April 1997 639 by guest on October 3, 2017 http://pediatrics.aappublications.org/ Downloaded from To determine risk factors for glue ear (serous otitis media), Black18 performed a case-control study of 150 children 4 to 9 years old undergoing myringotomy in Oxford, England. Children undergoing myringotomy were about 50% more likely to have lived in households where someone smoked than were control children. Hinton19 studied 115 children undergoing ear tube insertion for otitis media with effusion and a control group of 36 children from an orthoptic clinic. Children admitted for ear operations were more likely to have at least one parental smoker at home than the children in the control group. Etzel et al20 studied 132 children in a day care center to determine whether passive smoking was associated with an increased risk of middle ear effusion during the 18-month period between 6 and 24 months of age. In this study, the children were classified as exposed or not exposed to cigarette smoke on the basis of serum cotinine concentrations at 1 year of age. Middle ear effusion was diagnosed with the use of pneumatic otoscopy. The 45 children exposed to environmental tobacco smoke had an average of 7.1 episodes of middle ear effusion between 6 and 24 months of age, whereas the 87 children unexposed to environmental tobacco smoke had 5.8 episodes during that period. The average duration of middle ear effusion was 28 days among those in the exposed group and 19 days among those in the unexposed group. An estimated 8% of the middle ear effusions were attributed to exposure to environmental tobacco smoke. Strachan et al21 studied the relationship between passive smoking and middle ear effusion in 736 7-year-old school children in Edinburgh. In this study, investigators used objective measures of passive smoking and middle ear effusion, salivary cotinine concentrations, and impedance tympanometry. Children with type B tympanograms in one or both ears were categorized as having middle ear effusions. The results of this study indicated that detectable salivary cotinine was associated with type B tympanograms, even after adjustment for sex and the type of housing in which the children lived (rented versus owned). The authors estimated that at least one third of the cases of middle ear effusion among children in this age group may have been attributable to passive smoking. Owen and colleagues22 monitored 435 healthy children by tympanometry in the home every 2 to 4 weeks until 2 years of age. Of the children, 41% were exposed to household cigarette smoke. The authors found a significant association between the number of cigarettes smoked by household members and the frequency of otitis media with effusion during the second year of life. Ey and colleagues23 found that heavy maternal smoking (20 or more cigarettes per day) was a significant risk factor for recurrent otitis media during the first year of life. No association was found with paternal smoking. Passive Smoking and Asthma Children with asthma whose parents smoke may have more frequent exacerbations and more severe symptoms.24–35 In one of the few interventions reported in the literature, Murray and Morrison30 demonstrated that if parents expose their children with asthma to less cigarette smoke, the asthmatic symptoms the children have will be less severe. Passive Smoking and Sudden Infant Death Syndrome A growing body of evidence links exposure to environmental tobacco smoke to sudden infant death syndrome.36–48 This relationship seems to be independent of birth weight and gestational age. Passive Smoking and Lipid Profiles Passive smoking has also been reported to alter lipid profiles in adolescents. Feldman et al49 studied 391 nonsmoking adolescent students and found that those with elevated plasma cotinine concentrations had an 8.9% greater ratio of total cholesterol to highdensity lipoprotein cholesterol and 6.8% lower highdensity lipoprotein cholesterol than those with lower plasma cotinine concentrations. This may shed light on the mechanism of increased risk of coronary heart disease in passive smokers. Passive Smoking and Cancer Many studies link passive smoking to lung cancer in nonsmoking adults living with spouses who smoke.50–57 The US Environmental Protection Agency9 reviewed this subject and concluded that environmental tobacco smoke is a group A human carcinogen, the classification used when sufficient evidence from epidemiologic studies exists to support a causal association between exposure and cancer. A small number of studies have examined the relationship between exposure to environmental tobacco smoke during childhood and cancer risk. Sandler and colleagues58 found that the overall cancer risk was greater for individuals with exposures to environmental tobacco smoke during both childhood and adulthood than for individuals with exposure during only one period. When specific cancer sites or ty

There has been increasing interest in a targeted approach to the screening and prevention of lead exposure in children. Targeted screening requires an understanding of variation in lead exposure in individual children or by region. In order to better understand variation by region, we studied Rhode Island lead poisoning screening data, examining average lead exposure to children living in 136 Providence County census tracts (CTs). The study population included 17,956 children aged 59 months and under, who were screened between May 1, 1992, and April 30, 1993. We evaluated the relationship between the percentage of children with blood lead ≥10 μg/dL (pe10) and sociodemographic and housing characteristics, derived from United States 1990 Census data, of these CTs. CT descriptors included population density, percentage of households receiving public assistance income, median per capita income, percentage of households female headed, percentage of houses owner occupied, percentage of houses built before 1950, percentage of houses vacant, percentage of population Black, percentage of recent immigrants, and intraurban mobility. On average, 109 children were screened in each census tract; mean screening rate was 44%. There was wide variation in average lead exposure among census tracts, with pe10 ranging from 3 to 60% of screened children (mean 27%). Individual census variables explained between 24 and 67% of the variance in pe10 among CTs. A multiple regression model including percentage screened, percentage of households receiving public assistance, percentage of houses built before 1950, ln (percentage of houses vacant), and percentage of recent immigrants explained 83% of variance in pe10. The percentage of houses built before 1950, a variable which models the presence of lead paint in old houses, displayed the largest adjusted effect on pe10 over the range observed for that variable in RI CTs. The percentage of houses vacant was also a highly significant and robust predictor; we suggest that vacancy is an ecological marker for the deterioration of lead-based paint, with higher vacancy neighborhoods containing houses in poorer condition. In Rhode Island, census tracts with high vacancy rates also have high rates of recent immigration, making immigrant groups vulnerable to lead exposure. Small-areas analysis may be useful in directing resources to high risk areas, explaining the sociocultural forces which produce such exposure and analyzing the effects of housing policy over time in states with high screening penetration.

Noise is ubiquitous in our environment. High intensities of noise have been associated with numerous health effects in adults, including noise-induced hearing loss and high blood pressure. The intent of this statement is to provide pediatricians and others with information on the potential health effects of noise on the fetus and newborn. The information presented here supports a number of recommendations for both pediatric practice and government policy.

Blood lead concentrations in children have decreased dramatically in the last 20 years pari passu with the decrease in the amount of lead used in gasoline nationwide. The NHANES study of 1988-91 reported that the incidence of lead concentrations ≥ 25 μg/dL had fallen to 0.5% nationally. Blood Pb values in Northeast continued to be greater than in the rest of the country(33% greater than in the Midwest and over 200% those in the south and west of the US). However, the level in Massachusetts was similar to the national average. To explain the lower blood Pb in MA than in neighboring states, we compared average measures of childhood lead exposure in census tracts from Worcester County, MA, and Providence County, RI. These counties are geographically close, similar in metropolitan size, demographics, climate, and air lead concentrations. Pre-1950's houses comprise 45% of Worcester and 50% of Providence county housing stock. However, MA has aggressively enforced legal requirements for abatement of housing lead paint hazards since 1973. RI has had no legal abatement requirements before 1992. Both states have laws which require universal screening of young children. In a small areas analysis, we calculated mean blood lead in each of 154 census tracts (CTs) from Worcester County, MA (9787 children, 0-4 years, screened in 1993), and 136 Providence County, RI CTs (17982 children, 0-4 years, screened in 1994). We hypothesized that mean blood lead would be higher among RI CTs even after controlling for differences in US 1990 census-derived demographics and housing characteristics because of the cumulative effects of MA housing policy. Blood lead was ≥ 25 μg/dL in 0.5% of MA children and 5.2% of RI children. Mean blood lead was 5.6 μg/dL (std dev = 1.3) in the average MA CT, whereas it was 8.3 μg/dL (std dev = 2.4) in the average RI CT, an unadjusted difference 2.7 μg/dL. After adjusting for 12 sociodemographic and housing variables with multiple regression analysis, mean blood Pb in children in the average RI CT remained 33% higher than in the average MA CT (1.8 μg/dL, p<.0001). The MA-RI difference is completely explained by a significantly higher slope coefficient for the predicted relationship between pre-1950's housing in RI (β=0.050 in old RI houses) vs MA (β=0.014 in old MA houses), suggesting that this adjusted RI-MA difference is due to factors associated with old housing, of which the leading candidate factor is the cumulative effects of 23 years of enforced abatement of lead hazards in MA homes. Confirmation of this finding would have major policy implications. However, direct measurement of housing variables which model abatement will be necessary to confirm this premise.

This Policy Statement was retired January 2005. Child labor is the paid employment of children under 18 years of age. Today, more than 4 million children and adolescents in the United States are legally employed.1 Illegal child labor is also widespread and apparently has increased in frequency over the past decade. An estimated 1 to 2 million American children and adolescents are employed under unlawful, often exploitative conditions—working under age, for long hours, at less than minimum wage, on dangerous, prohibited machinery. Widespread employment of children in sweatshops—establishments that repeatedly violate fair labor as well as occupational health and safety standards—has been documented.2,3 Tens of thousands of children are employed in illegal farm labor. Detected violations of child labor laws increased fourfold from 1983 to 1989.4 LEGAL CONTEXT Since 1938, child labor in the United States has been regulated under the federal Fair Labor Standards Act (FLSA).5 Under this Act, employment in any hazardous nonagricultural occupation is prohibited for all children less than 18 years old. No child under 18 may work in mining, logging, construction, on a motor vehicle, or with power-driven machinery. The Act imposes additional restrictions on the employment of children under age 16 and sets limits on the number of hours a child may work on school days (no more than 3 hours per day for 14- and 15-year-olds). In agriculture, where legal restrictions are much less stringent, work with power-driven equipment and hazardous pesticides is prohibited only until age 16, and all work on family farms is exempt from legal protection. Work permits are a central aspect of the administration of FLSA.

In its recent statement on lead poisoning1 the American Academy of Pediatrics (AAP) Committee on Environmental Health articulated recommendations for screening that subtly but importantly differ from the approach currently being implemented by public health authorities across the nation. Universal screening for lead burden in children may be occurring in jurisdictions in which local data do not support this policy.2 The AAP noted significantly that there may exist low-risk communities that do not require screening, and locales in which selective screening of children is more appropriate than routine screening.1