Carbon monoxide exposures in New York City following Hurricane Sandy in 2012.

CONTEXT: On October 29, 2012, Hurricane Sandy made landfall and devastated New York's metropolitan area, causing widespread damage to homes and the utility infrastructure. Eight days later, snow and freezing temperatures from a nor'easter storm delayed utility restoration. OBJECTIVE: To examine carbon monoxide (CO) exposures in the 2 weeks following Hurricane Sandy. Methods. This was a retrospective review of prospectively collected, standardized, and de-identified data sets. CO exposures and poisonings identified from two electronic surveillance systems, the New York City Poison Control Center (NYCPCC) and New York City's Syndromic Surveillance Unit, were compared with CO exposures from identical dates in 2008-2011. Data collected from the poison center included exposure type, CO source, poisoning type, treatment, and outcomes. Data collected from the Syndromic Surveillance Unit cases, which were identified by CO-related chief complaints presenting to NYC hospitals, included visit date and time, and patient demographics. RESULTS: Four hundred thirty-seven CO exposures were reported to the NYCPCC, 355 from NYC callers, and the remainder from surrounding counties, which represented a significant increase when compared with CO exposures from identical dates in the preceding 4 years (p < 0.001). The total cases that were reported to the NYCPCC in 2008, 2009, 2010, and 2011 were 18, 13, 24, and 61, respectively. Excluding a single apartment fire that occurred (n = 311), the more common sources of CO were grilling indoors (26.2%) and generators (17.5%). Syndromic surveillance captured 70 cases; 6 cases were captured by both data sets. CONCLUSIONS: CO exposures following weather-related disasters are a significant public health concern, and the use of fuel-burning equipment is a clear source of storm-related morbidity and mortality. Multiple real-time epidemiologic surveillance tools are useful in estimating the prevalence of CO exposure and poisoning and are necessary to assist public health efforts to prevent CO poisoning during and after disasters.

Sociodemographic correlates of indoor allergen sensitivity among United States children.

BACKGROUND: Exposure to indoor allergens is associated with asthma morbidity. Nationally, asthma morbidity disproportionately affects socially disadvantaged populations, but it is unclear whether exposure to indoor allergens follows a similar pattern. OBJECTIVE: We sought to examine the national prevalences and demographic correlates of sensitivity to indoor allergens related to asthma. METHODS: Analysis of a cross-sectional survey of a representative sample of 4164 United States children aged 6 to 16 years who participated in allergen testing in the Third National Health and Nutrition Examination Survey from 1988 to 1994 was performed. The main outcome measures were sensitivity reactions to cockroach, dust mite, cat, and Alternaria alternata, as measured via skin prick testing. RESULTS: Multivariate models, including sex, age, race-ethnicity, education, poverty, family history, region of country, housing age, crowding, and urban residence, revealed significant racial-ethnic disparities in sensitivity. Compared with white children, African American children had higher odds ratios (ORs) of cockroach or dust mite sensitivity (cockroach OR, 2.5 [95% CI, 1.9-3.2]; dust mite OR, 1.3 [95% CI, 1.0-1.7]), as did Mexican American children (cockroach OR, 1.9 [95% CI, 1.3-2.8]; dust mite OR, 1.6 [95% CI, 1.2-2.2]). African American children also had significantly higher odds of sensitivity to A alternata (OR, 2.1 [95% CI, 1.5-2.8]). CONCLUSIONS: African American and Mexican American children are substantially more likely than white children to be sensitized to allergens important in asthma. Differences in indoor allergen sensitivity are consistent with racial differences in asthma morbidity. Along with other data, these findings suggest that racial disparities in housing, community, or both environmental factors play a role in determining national patterns of asthma morbidity.

Influence of variation in birth weight within normal range and within sibships on IQ at age 7 years: cohort study.

OBJECTIVE: To examine the relation between birth weight and measured intelligence at age 7 years in children within the normal range of birth weight and in siblings. DESIGN: Cohort study of siblings of the same sex. SETTING: 12 cities in the United States. SUBJECTS: 3484 children of 1683 mothers in a birth cohort study during the years 1959 through 1966. The sample was restricted to children born at >/=37 weeks gestation and with birth weights of 1500-3999 g. MAIN OUTCOME MEASURE: Full scale IQ at age 7 years. RESULTS: Mean IQ increased monotonically with birth weight in both sexes across the range of birth weight in a linear regression analysis of one randomly selected sibling per family (n= 1683) with adjustment for maternal age, race, education, socioeconomic status, and birth order. Within same sex sibling pairs, differences in birth weight were directly associated with differences in IQ in boys (812 pairs, predicted IQ difference per 100 g change in birth weight =0.50, 95% confidence interval 0.28 to 0.71) but not girls (871 pairs, 0.10, -0.09 to 0.30). The effect in boys remained after differences in birth order, maternal smoking, and head circumference were adjusted for and in an analysis restricted to children with birth weight >/= 2500 g. CONCLUSION: The increase in childhood IQ with birth weight continues well into the normal birth weight range. For boys this relation holds within same sex sibships and therefore cannot be explained by confounding from family social environment.

Evaluation of blood lead proficiency testing: comparison of open and blind paradigms.

BACKGROUND: Most proficiency testing (PT) programs operate with an open design in which clearly identified performance samples are distributed directly to participating laboratories on a shipping schedule announced in advance. In this study, we examine the effectiveness of assessing clinical laboratory performance for blood lead with an open PT by comparing its results with a double-blinded testing protocol. METHODS: Aliquots from up to 72 blood lead performance pools from the New York State Department of Health and the Wisconsin State Laboratory of Hygiene were disguised as routine patient specimens and submitted in two phases to up to 42 certified clinical laboratories for blood lead analysis. These 42 laboratories also received aliquots of the same performance samples for blood lead analysis directly from the "open" PT program provider. RESULTS: Data reported under blind and open strategies were scored against acceptable target ranges using the Clinical Laboratory Improvement Amendments of 1988 (CLIA '88) criteria established for blood lead, i.e., +/- 0.19 micromol/L (+/- 4 microg/dL) or +/- 10%, whichever is greater. Performance differences between the strategies were also assessed. We found that 17.7% of all blind PT results were classified as unacceptable compared with only 4.5% of open PT results (P <0.001). In phase 1, 13 of 22 laboratories (60%) exhibited a statistically significant difference (P <0.05) between their blind and open PT performances, although for 6 laboratories the poorer blind performance may not necessarily have led to unsuccessful PT participation under CLIA '88 criteria. Seven (32%) laboratories had unsuccessful aggregate performance (<80%) under blind testing while maintaining successful performance in open testing. Of these seven, two had gross discrepancies motivating further investigation. CONCLUSIONS: The data suggest that although approximately 60% of clinical laboratories make special efforts to improve analytical performance on open PT samples relative to performance achieved for routine patient specimens, in most cases the differences are clinically insignificant and would not likely affect cumulative PT performance. Occasional use of blind PT may deter the inclination to treat performance samples more carefully.

Housing and health--current issues and implications for research and programs.

This article provides an overview of the ways in which the home environment can affect human health, describes how specific health hazards in housing are related, and considers implications of these concerns for research and programs to address the health-housing connection. The widespread availability of decent housing has contributed greatly to improvements in health status in developed countries through, for example, provision of safe drinking water, proper sewage disposal, and protection from the elements. However, a lack of decent housing and homelessness among a significant number of Americans remains a significant public health concern. In addition, a number of specific health hazards can be found even in housing that is in good condition and provides all basic amenities. Specific health hazards related to housing include unintentional injuries, exposure to lead, exposure to allergens that may cause or worsen asthma, moisture and fungi (mold), rodent and insect pests, pesticide residues, and indoor air pollution. A number of these specific hazards share underlying causes, such as excess moisture, and all may be influenced by factors in the community environment or by occupant behaviors. We make recommendations for developing programs and research efforts that address multiple housing problems in an integrated way, rather than categorically, and for closer collaboration between housing and public health programs.

Elevated blood lead levels and blood lead screening among US children aged one to five years: 1988-1994.

OBJECTIVES: To estimate the proportion of children 1 to 5 years of age who received blood lead testing during 1988-1994 and to assess whether predictors of testing coincided with predictors of elevated blood lead levels. DESIGN: Cross-sectional analysis of data from the Third National Health and Nutrition Examination Survey. Participants. US children 1 to 5 years of age. Outcome Measures. Prevalence of blood lead testing and elevated blood lead levels among children 1 to 5 years of age and odds ratios for factors predicting blood lead testing and elevated blood lead levels. RESULTS: Overall, 6.3% had elevated blood lead levels and 10.2% had undergone previous blood lead tests. Being of minority race/ethnicity, living in an older home, residing in the Northeast or Midwest regions of the United States, being on Medicaid, having a head of household with <12 years of education, and having a history of anemia were significant factors in both models. Additional independent risk factors for an elevated blood lead level included being sampled in phase 1 of the survey, being 1 to 2 years of age, not having a regular doctor, and being sampled during the summer months. Additional independent correlates of a previous blood lead test included having moved less than twice in one's lifetime, having a female head of household, and having parents whose home language was English. Of an estimated 564 000 children 1 to 5 years of age who had elevated blood lead levels and no previous screening test in 1993, 62% were receiving Medicaid, 40% lived in homes built before 1946, and 34% were black, non-Hispanic. CONCLUSIONS: Lead screening was more frequent among children with risk factors for lead exposure. However, among children with elevated blood lead levels, only one third had been tested previously. In 1993 an estimated 564 000 children 1 to 5 years of age had elevated blood lead levels but were never screened. Physicians should screen Medicaid-eligible children and should follow state or local health department recommendations about identifying and screening other at-risk children. In areas where no health department guidelines exist, physicians should screen all children or screen based on known risk factors.

Children in Illinois with elevated blood lead levels, 1993-1998, and lead-related pediatric hospital admissions in Illinois, 1993-1997.

OBJECTIVE: This study uses screening and hospitalization data to describe the prevalence of childhood lead poisoning in Chicago and the rest of the state of Illinois. METHODS: The authors used aggregate data published by the Illinois Department of Public Health on blood lead testing of children ages 0-6 years and data on lead-related hospital admissions of children ages 0-6 years, drawn from an administrative dataset compiled as part of a state initiative. RESULTS: No clear time trends in the percentage of children with elevated blood lead levels (defined as >15 micrograms per deciliter [microg/dL] or >45 microg/dL) were evident in either Chicago or the rest of Illinois. The proportions of children with elevated blood lead levels in Chicago and in the rest of Illinois did not decline at the dramatic rate seen in the US as a whole during the 1990s. Over a five-year period, in-hospital charges of $7.7 million were generated for the care of lead-poisoned children ages 6-16 in Chicago alone. CONCLUSION: Surveillance data, analyzed at the appropriate geographic level, can be used to focus resources on high-risk areas and to evaluate prevention efforts.

Prenatal factors and adult mental and physical health.

OBJECTIVE: To review research on prenatal influences on adult mental and physical health and draw implications for future directions in psychiatric research. METHOD: Schizophrenia is selected as an example from mental health and cardiovascular disease as an example from physical health. For each of these disorders, empirical findings on prenatal influences are reviewed, and the methods used to demonstrate them are critiqued. RESULTS: Research on prenatal antecedents of these conditions has proceeded in parallel: intriguing findings have related fetal growth restriction or fetal insult to adult health; similar types of causal pathways have been proposed to explain the relationships; and research has been plagued by similar limitations, including lack of precise prenatal exposure data and difficulty of controlling confounding. The prevailing view of disease causation, which is not well-suited to investigation of prenatal antecedents, impedes research in both fields. Yet, there has been little interchange between researchers in the 2 fields. CONCLUSIONS: We propose a causal paradigm that could serve as a guide for future investigations on the prenatal antecedents of adult health and promote interchange between research on mental and physical health. The paradigm reflects current thinking in epidemiology by encompassing not only risk factors as traditionally conceived but also causal chains over time and causal influences at multiple levels of organization. Implications for the design of new research are illustrated with reference to an ongoing study.

Pesticides and inner-city children: exposures, risks, and prevention.

Six million children live in poverty in America's inner cities. These children are at high risk of exposure to pesticides that are used extensively in urban schools, homes, and day-care centers for control of roaches, rats, and other vermin. The organophosphate insecticide chlorpyrifos and certain pyrethroids are the registered pesticides most heavily applied in cities. Illegal street pesticides are also in use, including tres pasitos (a carbamate), tiza china, and methyl parathion. In New York State in 1997, the heaviest use of pesticides in all counties statewide was in the urban boroughs of Manhattan and Brooklyn. Children are highly vulnerable to pesticides. Because of their play close to the ground, their hand-to-mouth behavior, and their unique dietary patterns, children absorb more pesticides from their environment than adults. The long persistence of semivolatile pesticides such as chlorpyrifos on rugs, furniture, stuffed toys, and other absorbent surfaces within closed apartments further enhances urban children's exposures. Compounding these risks of heavy exposures are children's decreased ability to detoxify and excrete pesticides and the rapid growth, development, and differentiation of their vital organ systems. These developmental immaturities create early windows of great vulnerability. Recent experimental data suggest, for example, that chlorpyrifos may be a developmental neurotoxicant and that exposure in utero may cause biochemical and functional aberrations in fetal neurons as well as deficits in the number of neurons. Certain pyrethroids exert hormonal activity that may alter early neurologic and reproductive development. Assays currently used for assessment of the toxicity of pesticides are insensitive and cannot accurately predict effects to children exposed in utero or in early postnatal life. Protection of American children, and particularly of inner-city children, against the developmental hazards of pesticides requires a comprehensive strategy that monitors patterns of pesticide use on a continuing basis, assesses children's actual exposures to pesticides, uses state-of-the-art developmental toxicity testing, and establishes societal targets for reduction of pesticide use.

The contribution of lead-contaminated house dust and residential soil to children's blood lead levels. A pooled analysis of 12 epidemiologic studies.

In 1992, the U.S. Congress passed the Residential Lead-Based Paint Hazard Reduction Act, which requires the promulgation of health-based dust lead and soil lead standards for residential dwellings to prevent undue lead exposure in children. Unfortunately, the levels of lead in house dust and soil that are associated with elevated blood lead levels among U.S. children remain poorly defined. This pooled analysis was done to estimate the contributions of lead-contaminated house dust and soil to children's blood lead levels. The results of this pooled analysis, the most comprehensive existing epidemiologic analysis of childhood lead exposure, confirm that lead-contaminated house dust is the major source of lead exposure for children. These analyses further demonstrate that a strong relationship between interior dust lead loading and children's blood lead levels persists at dust lead levels considerably below the U.S. Department of Housing and Urban Development's current postabatement standards and the Environmental Protection Agency's guidance levels. Finally, these analyses demonstrate that a child's age, race, mouthing behaviors, and study-site specific factors influence the predicted blood lead level at a given level of exposure. These data can be used to estimate the potential health impact of alternative health-based lead standards for residential sources of lead exposure.

Elevated blood lead levels in children of construction workers.

OBJECTIVES: This study examined whether children of lead-exposed construction workers had higher blood lead levels than neighborhood control children. METHODS: Twenty-nine construction workers were identified from the New Jersey Adult Blood Lead Epidemiology and Surveillance (ABLES) registry. Eighteen control families were referred by workers. Venous blood samples were collected from 50 children (31 exposed, 19 control subjects) under age 6. RESULTS: Twenty-six percent of workers children had blood lead levels at or over the Centers for Disease Control and Prevention action level of 0.48 mumol/L (10 micrograms/dL), compared with 5% of control children (unadjusted odds ratio = 6.1; 95% confidence interval = 0.9, 147.2). CONCLUSIONS: Children of construction workers may be at risk for excessive lead exposure. Health care providers should assess parental occupation as a possible pathway for lead exposure of young children.

Lead-contaminated house dust and urban children's blood lead levels.

OBJECTIVES: This study assessed the relationship between lead-contaminated house dust and urban children's blood lead levels. METHODS: A random-sample survey was used to identify and enroll 205 children, 12 to 31 months of age, who had resided in the same house since at least 6 months of age. Children's blood and household dust, water, soil, and paint were analyzed for lead, and interviews were conducted to ascertain risk factors for elevated blood lead (> or = 10 micrograms/dL). RESULTS: Children's mean blood lead level was 7.7 micrograms/dL. In addition to dust lead loading (micrograms of lead per square foot), independent predictors of children's blood lead were Black race, soil lead levels, ingestion of soil or dirt, lead content and condition of painted surfaces, and water lead levels. For dust lead standards of 5 micrograms/sq ft, 20 micrograms/sq ft, and 40 micrograms/sq ft on noncarpeted floors, the estimated percentages of children having blood lead levels at or above 10 micrograms/dL were 4%, 15%, and 20%, respectively, after adjusting for other significant covariates. CONCLUSIONS: Lead-contaminated house dust is a significant contributor to lead intake among urban children who have low-level elevations in blood lead. A substantial proportion of children may have blood lead levels of at least 10 micrograms/dL at dust lead levels considerably lower than current standards.

Lead testing of children and homes: results of a national telephone survey.

OBJECTIVES: This study was designed to estimate the percentage of young children in the United States who have been tested for lead and the percentage of dwellings in the United States in which the paint has been tested for lead. METHODS: A national random digit dial telephone survey of 5238 households was conducted in 1994. Weighted national estimates and 95% confidence intervals for outcomes of interest were calculated. RESULTS: About 24% of U.S. children ages 0 to 6 years were estimated to have been tested for lead. Higher rates of testing were reported for children living in homes constructed prior to 1960, those living in homes with low household income, those living in rental units, and those living in the Northeast. Lead paint testing was performed for only an estimated 9% of U.S. housing units. Older homes were not more likely to have been tested than newer ones. CONCLUSION: A high proportion of pre-school children have apparently not been screened for lead exposure, even among subgroups at increased risk. Most dwellings of pre-school children have not been tested for lead paint. These data suggest that most at-risk children are not being reached by current approaches to lead poisoning prevention.

Acute high-dose lead exposure from beverage contaminated by traditional Mexican pottery.

Screening and follow-up blood lead measurements in a 7-year-old child of a US Embassy official in Mexico City revealed an increase in blood lead concentration from 1.10 to 4.60 mumol/L in less than 4 weeks. The cause was traced to fruit punch contaminated with lead leached from traditional ceramic pottery urns. Consumption of the contaminated punch at a picnic was associated with a 20% increase in blood lead concentrations among embassy staff and dependants who were tested 6 weeks after the exposure. This episode highlights the continued health risk, even from brief exposure, posed by traditional pottery in Mexico.

Blood lead levels in the US population. Phase 1 of the Third National Health and Nutrition Examination Survey (NHANES III, 1988 to 1991)

OBJECTIVE: To determine mean blood lead levels and their sociodemographic correlates in the US population. DESIGN: Nationally representative cross-sectional health examination survey that included measurements of venous blood lead. PARTICIPANTS: A total of 13,201 persons aged 1 year and older examined during phase 1 of the third National Health and Nutrition Examination Survey (1988 to 1991). RESULTS: The overall mean blood lead level for the US population was 0.14 mumol/L (2.8 micrograms/dL). Blood lead levels were consistently higher for younger children than for older children, for older adults than for younger adults, for males than for females, for blacks than for whites, and for central-city residents than for non-central-city residents. Other correlates of higher blood lead levels included low income, low educational attainment, and residence in the Northeast region of the United States. National estimates for children 1 to 5 years of age indicate that 8.9%, or approximately 1.7 million children, have blood lead levels 0.48 mumol/L (10 micrograms/dL) or greater. These levels are high enough to be of health concern under 1991 Centers for Disease Control and Prevention guidelines. CONCLUSIONS: The low overall mean blood lead levels demonstrate a major public health success in primary prevention efforts. However, exposure to lead at levels that may adversely affect the health of children remains a problem especially for those who are minority, urban, and from low-income families. Strategies to identify the most vulnerable risk groups are necessary to further reduce lead exposure in the United States.

The decline in blood lead levels in the United States. The National Health and Nutrition Examination Surveys (NHANES)

OBJECTIVE: To describe trends in blood lead levels for the US population and selected population subgroups during the time period between 1976 and 1991. DESIGN: Two nationally representative cross-sectional surveys and one cross-sectional survey representing Mexican Americans in the southwestern United States. SETTING/PARTICIPANTS: Participants in two national surveys that included blood lead measurements: the second National Health and Nutrition Examination Survey, 1976 to 1980 (n = 9832), and phase 1 of the third National Health and Nutrition Examination Survey, 1988 to 1991 (n = 12,119). Also, Mexican Americans participating in the Hispanic Health and Nutrition Examination Survey, 1982 to 1984 (n = 5682). RESULTS: The mean blood lead level of persons aged 1 to 74 years dropped 78%, from 0.62 to 0.14 mumol/L (12.8 to 2.8 micrograms/dL). Mean blood lead levels of children aged 1 to 5 years declined 77% (0.66 to 0.15 mumol/L [13.7 to 3.2 micrograms/dL]) for non-Hispanic white children and 72% (0.97 to 0.27 mumol/L [20.2 to 5.6 micrograms/dL]) for non-Hispanic black children. The prevalence of blood lead levels 0.48 mumol/L (10 micrograms/dL) or greater for children aged 1 to 5 years declined from 85.0% to 5.5% for non-Hispanic white children and from 97.7% to 20.6% for non-Hispanic black children. Similar declines were found in population subgroups defined by age, sex, race/ethnicity, income level, and urban status. Mexican Americans also showed similar declines in blood lead levels of a slightly smaller magnitude over a shorter time. CONCLUSIONS: The results demonstrate a substantial decline in blood lead levels of the entire US population and within selected subgroups of the population. The major cause of the observed decline in blood lead levels is most likely the removal of 99.8% of lead from gasoline and the removal of lead from soldered cans. Although these data indicate major progress in reducing lead exposure, they also show that the same sociodemographic factors continue to be associated with higher blood lead levels, including younger age, male sex, non-Hispanic black race/ethnicity, and low income level. Future efforts to remove other lead sources (eg, paint, dust, and soil) are needed but will be more difficult than removing lead from gasoline and soldered cans.

Long-term trends in blood lead levels among children in Chicago: relationship to air lead levels.

OBJECTIVES: To evaluate trends in blood lead levels among children in Chicago from 1968 through 1988, and to determine the impact of the changes in the Centers for Disease Control and Prevention (CDC) blood lead level of concern. METHODS: We reviewed a systematic sample of blood lead screening records of the Chicago Department of Health Laboratory for high-risk children aged 6 months to 5 years. Median blood lead levels for each quarter of the years 1974 through 1988 were determined and regressed against mean air lead levels recorded at air-monitoring stations in Chicago during the same period. RESULTS: Median blood lead levels declined from 30 micrograms/dL in 1968 to 12 micrograms/dL in 1988, and were strongly associated with declining average air lead levels (r = .8, P < .001) from 1974 through 1988. A regression model using log-transformed data predicted a decline of 0.56 microgram/dL in the median blood lead level with each 0.1 microgram/m3 decline in the mean air lead level when the air lead level was near 1.0 microgram/m3; the predicted slope was steeper at lower air lead levels. Despite the nearly 20-fold reduction in air lead levels, the median blood lead level of 12 micrograms/dL in 1988 indicates substantial continuing lead exposure. The CDC blood lead level of concern was lowered twice from 1968 to 1988, but due to the decline in blood lead levels, fewer than 30% of the children were above the level of concern throughout most of the study. CONCLUSION: Although substantial lead exposure persists in Chicago, reductions in airborne lead emissions seem to have contributed to a long-term decline in the median blood lead level of high-risk Chicago children.

Case-control study of congenital defects and parental employment in health care.

Health care workers may be occupationally exposed to known and suspected teratogens including viruses, anesthetic gases, sterilants, mercury, and x-radiation. To assess the risk of congenital defects among offspring of health care workers, we analyzed parental occupational histories for 4,915 case babies with congenital defects, registered during the years 1968-1980 by the Metropolitan Atlanta Congenital Defects Program (MACDP) registry, and for 3,027 control babies born without defects during the same period. Offspring of mothers employed in a nursing occupation during the periconceptional period had a modest excess risk of having at least one congenital defect (relative risk [RR] = 1.42; 95% confidence interval [CI] 1.06-1.88); the offspring were at statistically significant increased risk of having anencephaly or spina bifida (RR = 2.00; 95% CI 1.01-4.30), coarctation of the aorta (RR = 2.06; 95% CI 1.10-3.82), genital system defects (RR = 1.61; 95% CI 1.03-2.53), and urinary system defects (RR = 3.43; 95% CI 1.41-8.34). These associations were not confounded by maternal age, education, or alcohol consumption. Offspring of mothers employed in administrative or clerical jobs in the health care industry also had a modest excess risk of defects (RR = 1.35; 95% CI 0.96-1.90), including a statistically significant excess risk of limb defects. We also found associations between neural tube defects and potential exposure to anesthetic gases and to x-radiation, but each association was based on only three case babies of potentially exposed parents. We found no associations between defects and paternal health care employment, except for a few individual defects, and these were based on small numbers of exposed subjects. Only one of five previous studies reviewed found an increased risk of congenital defects among offspring of nurses, but three of the four negative studies had substantially smaller sample sizes than the present study. Detection bias may be a possible explanation for the apparent excess risk of certain defects among offspring of nurses.