ObjectiveTo examine associations between birth defects and cancer from birth into adulthood.DesignPopulation based nested case-control study.SettingNationwide health registries in Denmark, Finland, Norway, and Sweden.Participants62 295 cancer cases (0-46 years) and 724 542 frequency matched controls (matched on country and birth year), born between 1967 and 2014.Main outcome measuresRelative risk of cancer in relation to major birth defects, estimated as odds ratios with 99% confidence intervals from logistic regression models.ResultsAltogether, 3.5% (2160/62 295) of cases and 2.2% (15 826/724 542) of controls were born with major birth defects. The odds ratio of cancer for people with major birth defects compared with those without was 1.74 (99% confidence interval 1.63 to 1.84). For individuals with non-chromosomal birth defects, the odds ratio of cancer was 1.54 (1.44 to 1.64); for those with chromosomal anomalies, the odds ratio was 5.53 (4.67 to 6.54). Many structural birth defects were associated with later cancer in the same organ system or anatomical location, such as defects of the eye, nervous system, and urinary organs. The odds ratio of cancer increased with number of defects and decreased with age, for both non-chromosomal and chromosomal anomalies. The odds ratio of cancer in people with any non-chromosomal birth defect was lower in adults (≥20 years: 1.21, 1.09 to 1.33) than in adolescents (15-19 years: 1.58, 1.31 to 1.90) and children (0-14 years: 2.03, 1.85 to 2.23). The relative overall cancer risk among adults with chromosomal anomalies was markedly reduced from 11.3 (9.35 to 13.8) in children to 1.50 (1.01 to 2.24). Among adults, skeletal dysplasia (odds ratio 3.54, 1.54 to 8.15), nervous system defects (1.76, 1.16 to 2.65), chromosomal anomalies (1.50, 1.01 to 2.24), genital organs defects (1.43, 1.14 to 1.78), and congenital heart defects (1.28, 1.02 to 1.59) were associated with overall cancer risk.ConclusionsThe increased risk of cancer in individuals with birth defects persisted into adulthood, both for non-chromosomal and chromosomal anomalies. Further studies on the molecular mechanisms involved are warranted.

Purpose Workers on offshore petroleum installations are at risk of being exposed to benzene which is carcinogenic to humans. The present study aimed to assess the time trend of full-shift benzene exposure from 2002 to 2018 in order to characterize benzene exposure among laboratory technicians, mechanics, process operators, and industrial cleaners, and to examine the possible determinants of benzene exposure. Methods A total of 924 measurements of benzene exposure from the Norwegian petroleum offshore industry were included. The median sampling duration was 680 min, ranging from 60 to 940 min. The overall geometric mean (GM) and 95% confidence interval, time trends, and determinants of exposure were estimated using multilevel mixed-effects tobit regression analyses. Time trends were estimated for sampling duration below and above 8 h, both overall and for job groups. The variability of exposure between installation and workers was investigated in a subset of data containing worker identification. Results The overall GM of benzene exposure was 0.004 ppm. When adjusting for job group, design of process area, season, wind speed, and sampling duration, industrial cleaners had the highest exposure (GM = 0.012). Laboratory technicians, mechanics, and process operators had a GM exposure of 0.004, 0.003, and 0.004 ppm, respectively. Overall, the measured benzene exposure increased by 7.6% per year from 2002 to 2018. Mechanics had an annual increase of 8.6% and laboratory technicians had an annual decrease of 12.6% when including all measurements. When including only measurements above 8 h, mechanics had an increase of 16.8%. No statistically significant time trend was found for process operators. Open process area, high wind speed, and wintertime were associated with reduced exposure level. Conclusions An overall increase in measured exposure was observed from 2002 to 2018. The increase may reflect changes in measurement strategy from mainly measuring on random days to days with expected exposure. However, the time trend varied between job groups and was different for sampling duration above or below 8 h. Industrial cleaners had the highest exposure of the four job groups while no differences in exposure were observed between laboratory technicians, mechanics, and process operators. The design of the process area, job group, wind speed, and season were all significant determinants of benzene exposure.

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Background Childhood cancer is more common among children with birth defects, suggesting a common aetiology. Whether this association differs by sex is unclear. Methods We performed a population-based nested case-control study using nationwide health registries in four Nordic countries. We included 21 898 cancer cases (0–19 years) and 218 980 matched population controls, born 1967–2014. Associations between childhood cancer and major birth defects were calculated as odds ratios (ORs) with 95% confidence intervals (CIs) using logistic regression models. Effect modification was evaluated using a counterfactual framework to estimate confidence intervals and P-values for the natural indirect effects. Results Birth defects were present for 5.1% (1117/21 898) of childhood cancer cases and 2.2% (4873/218 980) of controls; OR of cancer was higher for chromosomal (OR = 10, 95% CI = 8.6–12) than for non-chromosomal defects (OR = 1.9, 95% CI = 1.8–2.1), strongest between genetic syndromes/microdeletion and renal tumours, Down syndrome and leukaemia, and nervous system defects and central nervous system tumours. The association between birth defects and cancer was stronger among females (OR = 2.8, 95% CI = 2.6–3.1) than males (OR = 2.1, 95% CI = 1.9–2.2, Pinteraction <0.001). Male sex was an independent risk factor for childhood cancer, but very little of the overall association between sex and childhood cancer was mediated through birth defects (4.8%, PNIE <0.001), although more at younger ages (10% below years and 28% below 1 year). Conclusions The birth defect–cancer associations were generally stronger among females than males. Birth defects did not act as a strong mediator for the modest differences in childhood cancer risk by sex, suggesting that other biological pathways are involved.