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1.  Birth weight and other perinatal characteristics and childhood leukemia in California 
Cancer epidemiology  2012;36(6):e359-e365.
We conducted a large registry-based study in California to investigate the association of perinatal factors and childhood leukemia with analysis of two major subtypes, acute lymphocytic leukemia (ALL) and acute myeloid leukemia (AML).
We linked California cancer and birth registries to obtain information on 5788 cases and 5788 controls matched on age and sex (1:1). We examined the association of birth weight, gestational age, birth and pregnancy order, parental ages, and specific conditions during pregnancy and risk of total leukemia, ALL and AML using conditional logistic regression, with adjustment for potential confounders.
The odds ratio (OR) per 1000 gram increase in birth weight was 1.11 for both total leukemia and ALL. The OR were highest for babies weighing ≥4,500g with reference <2,500g: 1.59 (95% CI: 1.05-2.40) and 1.70 (95% CI: 1.08-2.68) for total leukemia and ALL, respectively. For AML, increase in risk was also observed but the estimate was imprecise due to small numbers. Compared to average-for-gestational age (AGA), large-for-gestational age (LGA) babies were at slightly increased risk of total childhood leukemia (OR=1.10) and both ALL and AML (OR=1.07 and OR=1.13, respectively) but estimates were imprecise. Being small-forgestational age (SGA) was associated with reduced risk of childhood leukemia (OR=0.81, 95% CI: 0.67-0.97) and ALL (OR=0.77, 95% CI: 0.63-0.94), but not AML. Being first-born was associated with decreased risk of AML only (OR=0.70; 95% CI: 0.53-0.93). Compared to children with paternal age <25 years, children with paternal age between 35 and 45 years were at increased risk of total childhood leukemia (OR=1.12; 95% CI: 1.04-1.40) and ALL (OR=1.23; 95% CI: 1.04-1.47). None of conditions during pregnancy examined or maternal age were associated with increased risk of childhood leukemia or its subtypes.
Our results suggest that high birth weight and LGA were associated with increased risk and SGA with decreased risk of total childhood leukemia and ALL, being first-born was associated with decreased risk of AML, and advanced paternal age was associated with increased risk of ALL. These findings suggest that associations of childhood leukemia and perinatal factors depend highly on subtype of leukemia.
PMCID: PMC4034745  PMID: 22926338
childhood leukemia; birth weight; birth order; parental age; perinatal factors; pregnancy complications
2.  The incidence of leukemia, lymphoma, and multiple myeloma among atomic bomb survivors: 1950 – 2001 
Radiation research  2013;179(3):10.1667/RR2892.1.
A marked increase in leukemia risks was the first and most striking late effect of radiation exposure seen among the Hiroshima and Nagasaki atomic bomb survivors. This paper presents analyses of radiation effects on leukemia, lymphoma, and multiple myeloma incidence in the Life Span Study cohort of atomic bomb survivors updated 14 years since the last comprehensive report on these malignancies. These analyses make use of tumor- and leukemia-registry-based incidence data on 113,011 cohort members with 3.6 million person-years of follow-up from late 1950 through the end of 2001. In addition to a detailed analysis of the excess risk for all leukemias other than chronic lymphocytic leukemia or adult T-cell leukemia (neither of which appear to be radiation-related), we present results for the major hematopoietic malignancy types: acute lymphoblastic leukemia, chronic lymphocytic leukemia, acute myeloid leukemia, chronic myeloid leukemia, adult T-cell leukemia, Hodgkin and non-Hodgkin lymphoma, and multiple myeloma. Poisson regression methods were used to characterize the shape of the radiation dose response relationship and, to the extent the data allowed, to investigate variation in the excess risks with sex, attained age, exposure age, and time since exposure. In contrast to the previous report that focused on describing excess absolute rates, we considered both excess absolute rate (EAR) and excess relative risk (ERR) models and found that ERR models can often provide equivalent and sometimes more parsimonious descriptions of the excess risk than EAR models. The leukemia results indicated that there was a non-linear dose response for leukemias other than chronic lymphocytic leukemia or adult T-cell leukemia, which varied markedly with time and age at exposure, with much of the evidence for this non-linearity arising from the acute myeloid leukemia risks. Although the leukemia excess risks generally declined with attained age or time since exposure, there was evidence that the radiation-associated excess leukemia risks, especially for acute myeloid leukemia, had persisted throughout the follow-up period out to – 55 years after the bombings. As in earlier analyses, there was a weak suggestion of a radiation dose response for non-Hodgkin lymphoma among men with no indication of such an effect among women. There was no evidence of radiation-associated excess risks for either Hodgkin lymphoma or multiple myeloma.
PMCID: PMC3875218  PMID: 23398354
3.  Long-Term Use of Acetaminophen, Aspirin, and Other Nonsteroidal Anti-Inflammatory Drugs and Risk of Hematologic Malignancies: Results From the Prospective Vitamins and Lifestyle (VITAL) Study 
Journal of Clinical Oncology  2011;29(17):2424-2431.
Among previous studies examining the associations of over-the-counter analgesics or nonsteroidal anti-inflammatory drugs (NSAIDs) and incident hematologic malignancies, results were inconsistent for NSAIDs but suggested an increased risk with acetaminophen (paracetamol). Herein, we used a large prospective cohort study to examine these associations.
Patients and Methods
In total, 64,839 men and women age 50 to 76 years were recruited from 2000 to 2002 to the Vitamins and Lifestyle (VITAL) study. Incident hematologic malignancies (n = 577) were identified through December 2008 by linkage to the Surveillance, Epidemiology and End Results cancer registry. Hazard ratios (HRs) associated with use of analgesics for total incident hematologic malignancies and cancer subcategories were estimated by Cox proportional hazards models. Models were adjusted for age, sex, race/ethnicity, education, smoking, self-rated health, arthritis, chronic musculoskeletal pain, migraines, headaches, fatigue, and family history of leukemia/lymphoma.
After adjustment, there was an increased risk of incident hematologic malignancies associated with high use (≥ 4 days/week for ≥ 4 years) of acetaminophen (HR, 1.84; 95% CI, 1.35 to 2.50 for high use; P trend = .004). This association was seen for myeloid neoplasms (HR, 2.26; 95% CI, 1.24 to 4.12), non-Hodgkin's lymphomas (HR, 1.81; 95% CI, 1.12 to 2.93), and plasma cell disorders (HR, 2.42; 95% CI, 1.08 to 5.41), but not chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL; HR, 0.84; 95% CI, 0.31 to 2.28). By comparison, there was no association with risk of incident hematologic malignancies for increasing use of aspirin, nonaspirin NSAIDs, or ibuprofen.
High use of acetaminophen was associated with an almost two-fold increased risk of incident hematologic malignancies other than CLL/SLL. Neither aspirin nor nonaspirin NSAIDs are likely useful for prevention of hematologic malignancies.
PMCID: PMC3107756  PMID: 21555699
4.  Perinatal and Family Risk Factors for Non-Hodgkin Lymphoma in Early Life: A Swedish National Cohort Study 
The incidence of non-Hodgkin lymphoma (NHL) in early life has increased in recent decades, but the relevant risk factors remain largely unknown. We examined perinatal and family risk factors for NHL in childhood through young adulthood.
We conducted a national cohort study of 3 571 574 individuals born in Sweden in 1973–2008 who were followed for incidence of NHL through 2009 (ages 0–37 years). Detailed information on perinatal and family characteristics and NHL diagnoses were obtained from national birth and cancer registries. Cox proportional hazards regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between perinatal and family variables and NHL; P values are from two-sided tests.
There were 936 NHL case patients identified in 66.3 million person-years of follow-up. Independent risk factors for NHL included family history of NHL in either a sibling (adjusted HR = 9.84; 95% CI = 2.46 to 39.41; P = .001) or parent (adjusted HR = 2.36; 95% CI = 1.27 to 4.38; P = .007); high fetal growth (for ≥2 SDs relative to 0 to <1 SD from the mean: adjusted HR = 1.64; 95% CI = 1.19 to 2.25; P = .002); older maternal age (adjusted HR for each 5-year increment = 1.11; 95% CI = 1.04 to 1.19; P trend = .004); low birth order (adjusted HR for each increment of one birth = 0.91; 95% CI = 0.84 to 0.99; P trend = .02); and male sex (adjusted HR = 1.58; 95% CI = 1.38 to 1.80; P < .001). Male sex was associated with onset of NHL before 15 years of age but not with later-onset NHL, whereas the other risk factors did not vary by age at diagnosis. No association was found between gestational age at birth, twinning, paternal age, or parental education and NHL.
In this large national cohort study, family history of NHL, high fetal growth, older maternal age, low birth order, and male sex were independent risk factors for NHL in early life.
PMCID: PMC3732249  PMID: 22623506
5.  Parental age and risk of childhood cancer: A pooled analysis 
Epidemiology (Cambridge, Mass.)  2009;20(4):475-483.
Few risk factors for childhood cancer are well-established. We investigated whether advancing parental age increases childhood cancer risk.
We assessed the relationship between parental age and childhood cancer in a case-control study using pooled population-based data. Our pooling was based on linked cancer and birth registry records from New York, Washington, Minnesota, Texas, and California. Subjects included 17,672 cancer cases diagnosed at ages 0–14 years during 1980–2004 and 57,966 controls born during 1970–2004. Persons with Down syndrome were excluded. Odds ratios and 95% confidence intervals were calculated by logistic regression for the association between parental age and childhood cancer after adjustment for sex, birth weight, gestational age, birth order, plurality, maternal race, birth year, and state.
Positive linear trends per 5-year maternal age increase were –observed for childhood cancers overall (odds ratio = 1.08 [95% confidence interval = 1.06–1.10]) and 7 of the 10 most frequent diagnostic groups: leukemia (1.08 [1.05–1.11]), lymphoma (1.06 [1.01–1.12]), central nervous system tumors (1.07 [1.03–1.10]), neuroblastoma (1.09 [1.04–1.15]), Wilms’ tumor (1.16 [1.09–1.22]), bone tumors (1.10 [ 1.00–1.20]), and soft tissue sarcomas (1.10 [1.04–1.17]). No maternal age effect was noted for retinoblastoma, germ cell tumors, or hepatoblastoma. Paternal age was not independently associated with most childhood cancers after adjustment for maternal age.
Our results suggest that older maternal age increases risk for most common childhood cancers. Investigation into possible mechanisms for this association is warranted.
PMCID: PMC2738598  PMID: 19373093
6.  Paternal age at birth is associated with offspring leukocyte telomere length in the nurses' health study 
Human Reproduction (Oxford, England)  2012;27(12):3622-3631.
Is the association between paternal age at birth and offspring leukocyte telomere length (LTL) an artifact of early life socioeconomic status (SES)?
Indicators of early life SES did not alter the relationship between paternal age at birth and offspring LTL among a population of white female nurses.
Telomere length is considered a highly heritable trait. Recent studies report a positive correlation between paternal age at birth and offspring LTL. Maternal age at birth has also been positively associated with offspring LTL, but may stem from the strong correlation with paternal age at birth.
The Nurses' Health Study (NHS) is an ongoing prospective cohort study of 121 700 female registered nurses who were enrolled in 1976. Great effort goes into maintaining a high degree of follow-up among our cohort participants (>95% of potential person-years). In 1989–1990, a subset of 32 826 women provided blood samples from which we selected participants for several nested case–control studies of telomere length and incident chronic disease. We used existing LTL data on a total of 4250 disease-free women who also reported maternal and paternal age at birth for this study.
Nested case–control studies of stroke, myocardial infarction, cancers of the breast, endometrium, skin, pancreas and colon, as well as colon adenoma, were conducted within the blood sub-cohort. Each study used the following study design: for each case of a disease diagnosed after blood collection, a risk-set sampling scheme was used to select from one to three controls from the remaining participants in the blood sub-cohort who were free of that disease when the case was diagnosed. Controls were matched to cases by age at blood collection (±1 year), date of blood collection (±3 months), menopausal status, recent postmenopausal hormone use at blood collection (within 3 months, except for the myocardial infarction case–control study), as well as other factors carefully chosen for each individual study. The current analysis was limited to healthy controls. We also included existing LTL data from a small random sample of women participating in a cognitive sub-study. LTL was measured using the quantitative PCR-based method. Exposure and covariate information are extracted from biennial questionnaires completed by the participants.
We found a strong association between paternal age at birth and participant LTL (P = 1.6 × 10–5) that remained robust after controlling for indicators of early life SES. Maternal age at birth showed a weak inverse association with participant LTL after adjusting for age at blood collection and paternal age at birth (P = 0.01). We also noted a stronger association between paternal age at birth and participant LTL among premenopausal than among postmenopausal women (Pinteraction = 0.045). However, this observation may be due to chance as premenopausal women represented only 12.6% (N = 535) of the study population and LTL was not correlated with age at menopause, total or estrogen-only hormone therapy (HT) use suggesting that changes in in vivo estrogen exposure do not influence telomere length regulation.
The women in our study are not representative of the general US female population, with an underrepresentation of non-white and low social class groups. Although the interaction was not significant, we noted that the paternal age at birth association with offspring LTL appeared weaker among women whose parents did not own their home at the time of the participant's birth. As telomere dynamics may differ among individuals who are most socioeconomically deprived, SES indicators may have more of an influence on the relationship between paternal age at birth and offspring LTL in such populations.
As of yet, our and prior studies have not identified childhood or adult characteristics that confound the paternal age at birth association with offspring LTL, supporting the hypothesis that offspring may inherit the longer telomeres found in sperm of older men. The biological implications of the paternal age effect are unknown. A recent theory proposed that the inheritance of longer telomere from older men may be an adaptive signal of reproductive lifespan, while another theory links telomere length attrition to female reproductive senescence. However, we are unaware of any data to substantiate a relationship between paternal age at birth and daughter's fertility. Generalizability of our study results to other white female populations is supported by prior reports of paternal age at birth and offspring telomere length. Furthermore, a confounding relationship between paternal or maternal age at birth and SES was not observed in a study of SES and telomere length.
This work was supported by the National Institutes of Health (grants numbers: CA87969, CA49449, CA065725, CA132190, CA139586, HL088521, CA140790, CA133914, CA132175, ES01664 to M.D.); and by the American Health Association Foundation. We have no competing interests to declare.
PMCID: PMC3501241  PMID: 22940768
epidemiology; telomere; paternal age; maternal age; social class
7.  Household Exposure to Pesticides and Risk of Childhood Hematopoietic Malignancies: The ESCALE Study (SFCE) 
Environmental Health Perspectives  2007;115(12):1787-1793.
We investigated the role of household exposure to pesticides in the etiology of childhood hematopoietic malignancies.
The national registry-based case–control study ESCALE (Etude sur les cancers de l’enfant) was carried out in France over the period 2003–2004. Population controls were frequency matched with the cases on age and sex. Maternal household use of pesticides during pregnancy and paternal use during pregnancy or childhood were reported by the mothers in a structured telephone questionnaire. Insecticides (used at home, on pets, or for garden crops), herbicides, and fungicides were distinguished. We estimated odds ratios (ORs) using unconditional regression models closely adjusting for age, sex, degree of urbanization, and type of housing (flat or house).
We included a total of 764 cases of acute leukemia (AL), 130 of Hodgkin lymphoma (HL), 166 of non-Hodgkin lymphoma (NHL), and 1,681 controls. Insecticide use during pregnancy was significantly associated with childhood AL [OR = 2.1; 95% confidence interval (CI), 1.7–2.5], both lymphoblastic and myeloblastic, NHL (OR = 1.8; 95% CI, 1.3–2.6), mainly for Burkitt lymphoma (OR = 2.7; 95% CI, 1.6–4.5), and mixed-cell HL (OR = 4.1; 95% CI, 1.4–11.8), but not nodular sclerosis HL (OR = 1.1; 95% CI, 0.6–1.9). Paternal household use of pesticides was also related to AL (OR = 1.5; 95% CI, 1.2–1.8) and NHL (OR = 1.7; 95% CI, 1.2–2.6); but for AL the relationships did not remain after adjustment for maternal pesticide use during pregnancy.
The study findings strengthen the hypothesis that domestic use of pesticides may play a role in the etiology of childhood hematopoietic malignancies. The consistency of the findings with those of previous studies on AL raises the question of the advisability of preventing pesticide use by pregnant women.
PMCID: PMC2137105  PMID: 18087601
acute leukemia; children; Hodgkin lymphoma; non-Hodgkin lymphoma; pesticide; pregnancy
8.  Body Size, Recreational Physical Activity, and B-Cell Non-Hodgkin Lymphoma Risk Among Women in the California Teachers Study 
American Journal of Epidemiology  2009;170(10):1231-1240.
Nutritional status and physical activity are known to alter immune function, which may be relevant to lymphomagenesis. The authors examined body size measurements and recreational physical activity in relation to risk of B-cell non-Hodgkin lymphoma (NHL) in the prospective California Teachers Study. Between 1995 and 2007, 574 women were diagnosed with incident B-cell NHL among 121,216 eligible women aged 22–84 years at cohort entry. Multivariable-adjusted relative risks and 95% confidence intervals were estimated by fitting Cox proportional hazards models for all B-cell NHL combined and for the 3 most common subtypes: diffuse large B-cell lymphoma, follicular lymphoma, and B-cell chronic lymphocytic leukemia/small lymphocytic lymphoma. Height was positively associated with risk of all B-cell NHLs (for >1.70 vs. 1.61–1.65 m, relative risk = 1.50, 95% confidence interval: 1.16, 1.96) and chronic lymphocytic leukemia/small lymphocytic lymphoma (relative risk = 1.93, 95% confidence interval: 1.09, 3.41). Weight and body mass index at age 18 years were positive predictors of B-cell NHL risk overall. These findings indicate that greater height, which may reflect genetics, early life immune function, infectious exposures, nutrition, or growth hormone levels, may play a role in NHL etiology. Adiposity at age 18 years may be more relevant to NHL etiology than that in later life.
PMCID: PMC2781760  PMID: 19822569
body mass index; body size; cohort studies; exercise; hip; lymphoma, non-Hodgkin; waist-hip ratio
9.  Presence of Simian Virus 40 DNA Sequences in Egyptian Patients with Lymphoproliferative Disorders 
Although no definite risk factors have emerged for the different hematological malignancies, a viral cause has been postulated. Several studies have detected SV40 DNA sequences in tumor tissues obtained from non-Hodgkin’s lymphoma patients. A link between SV40 and NHL is biologically plausible because SV40 causes hematological malignancies in laboratory rodents.
We investigated 266 Egyptian cases of different hematological malignancies, for the presence of SV40 DNA using multiplex nested PCR technique. These cases consisted of 158 non-Hodgkin’s lymphoma (NHL), 54 Hodgkin’s disease(HD), 26 acute lymphocytic leukemia (ALL), 13 acute myeloid leukemia (AML), 8 chronic lymphoblastic leukemia (CLL), 7 chronic myeloid leukemia (CML), in addition to 34 subjects of control group.
Our results have shown that SV40 DNA sequences were found in 53.8% of non-Hodgkin lymphoma patients, 29.6% of Hodgkin’s disease patients, and 40.7% of different types of leukemia cases. Frequency of SV40 DNA sequences was higher in NHL patients compared to the other tumor cases. Also, frequency of SV40 DNA sequences was significantly higher (p<0.05) in NHL patients than in the control group. Regarding the different histological types of non-Hodgkin’s lymphoma, SV40 DNA sequences were detected frequently in diffuse large B-cell lymphoma and in follicular lymphoma.
The present study suggests that SV40 DNA virus is significantly associated with non-Hodgkin’s lymphoma and might have a role in the development of these hematological malignancies. Polyomavirus SV40 may act as a cofactor in the pathogenesis of these tumors and this could lead to new diagnostic, therapeutic, and preventive approaches.
PMCID: PMC3068659  PMID: 21475447
10.  Advanced paternal and grandpaternal age and schizophrenia: A three-generation perspective 
Schizophrenia research  2011;133(0):120-124.
Advanced paternal age has been linked with neurodevelopmental disorders such as schizophrenia. If age-related de novo mutations in the male germ line underlie this association, it would be expected that grandpaternal as well as paternal age may influence the risk of schizophrenia. The aim of the current study was to explore the links between both paternal and grandpaternal age with respect to the risk of schizophrenia in a large, national register-based sample.
The study was based on Swedish Multi-Generation and Hospital Discharge Registers. Parents’ ages at offspring birth were compared between 20,582 affected and 100,176 non-affected individuals. Grandparents’ ages at the birth of the parent were compared between 2,511 affected and 15,619 non-affected individuals. The risk of schizophrenia was examined when the predictor variable (parent or grandparent age) was examined in age strata with logistic regression. Planned sensitivity analyses included exploring the variables of interest in males and females separately.
After adjusting for maternal age, birth year and sex of the proband, we confirmed that the offspring of older fathers have an increased risk of schizophrenia (e.g. compared to paternal age 20–24 years, those with fathers > 55 years had a two-fold increased risk). With respect to grandparent age, older maternal (but not paternal) grandfather age was associated with an increased risk of schizophrenia. Compared to maternal grandfather age 20–24 years, those with maternal grandfathers >55 years had a significantly increased risk of schizohrpenia (Adjusted Odds ratio and 95% Confidence intervals; 2.79, 1.71 – 4.56). The pattern of findings were essentially unchanged when we examine male and female probands separately.
This is the first the study to show an association between grandpaternal age and risk of schizophrenia. The selective effect of advanced maternal grandfather age suggests that the biological mechanisms involving the X chromosome may differentially contribute to the association between paternal age and risk of schizophrenia.
PMCID: PMC3660090  PMID: 22000939
schizophrenia; paternal age; grandparental age; mutation
11.  Results of case-control study of leukaemia and lymphoma among young people near Sellafield nuclear plant in West Cumbria. 
BMJ : British Medical Journal  1990;300(6722):423-429.
OBJECTIVE--To examine whether the observed excess of childhood leukaemia and lymphoma near the Sellafield nuclear plant is associated with established risk factors or with factors related to the plant. DESIGN--A case-control study. SETTING--West Cumbria health district. SUBJECTS--52 Cases of leukaemia, 22 of non-Hodgkin's lymphoma, and 23 of Hodgkin's disease occurring in people born in the area and diagnosed there in 1950-85 under the age of 25 and 1001 controls matched for sex and date of birth taken from the same birth registers as the cases. MAIN OUTCOME MEASURES--Antenatal abdominal x ray examinations, viral infections, habit factors, proximity to and employment characteristics of parents at Sellafield. RESULTS--Expected associations with prenatal exposure to x rays were found, but little information was available on viral illnesses. Relative risks for leukaemia and non-Hodgkin's lymphoma were higher in children born near Sellafield and in children of fathers employed at the plant, particularly those with high radiation dose recordings before their child's conception. For example, the relative risks compared with area controls were 0.17 (95% confidence interval 0.05 to 0.53) for being born further than 5 km from Sellafield 2.44 (1.04 to 5.71) for children of fathers employed at Sellafield at their conception, and 6.42 (1.57 to 26.3) for children of fathers receiving a total preconceptual ionising radiation dose of 100 mSv or more. Other factors, including exposure to x rays, maternal age, employment elsewhere, eating seafood, and playing on the beach did not explain these relationships. Focusing on Seascale, where the excess incidence has predominantly been reported, showed for the four out of five cases of leukaemia and one case of non-Hodgkin's lymphoma whose fathers were employed at Sellafield and for whom dose information was obtained that the fathers of each case had higher radiation doses before their child's conception than all their matched control fathers; the father of the other Seascale case (non-Hodgkin's lymphoma) was not employed at the plant. These results seem to explain statistically the geographical association. For Hodgkin's disease neither geographical nor employment associations with Sellafield were found. CONCLUSIONS--The raised incidence of leukaemia, particularly, and non-Hodgkin's lymphoma among children near Sellafield was associated with paternal employment and recorded external dose of whole body penetrating radiation during work at the plant before conception. The association can explain statistically the observed geographical excess. This result suggests an effect of ionising radiation on fathers that may be leukaemogenic in their offspring, though other, less likely, explanations are possible. There are important potential implications for radiobiology and for protection of radiation workers and their children.
PMCID: PMC1662259  PMID: 2107892
12.  Cancer Disparities in the Context of Medicaid Insurance: A Comparison of Survival for Acute Myeloid Leukemia and Hodgkin's Lymphoma by Medicaid Enrollment 
The Oncologist  2011;16(8):1082-1091.
Using Medicaid enrollment as a proxy for poverty, potential disparities in survival after a diagnosis of acute myeloid leukemia or Hodgkin's lymphoma were assessed in a nonelderly population. Poverty did not affect survival for acute myeloid leukemia patients but did appear to be associated with survival for Hodgkin's lymphoma patients.
Because poverty is difficult to measure, its association with outcomes for serious illnesses such as hematologic cancers remains largely uncharacterized. Using Medicaid enrollment as a proxy for poverty, we aimed to assess potential disparities in survival after a diagnosis of acute myeloid leukemia (AML) or Hodgkin's lymphoma (HL) in a nonelderly population.
We used records from the New York (NY) and California (CA) state cancer registries linked to Medicaid enrollment records for these states to identify Medicaid enrolled and nonenrolled patients aged 21–64 years with incident diagnoses of AML or HL in 2002–2006. We compared overall survival for the two groups using Kaplan–Meier curves and Cox proportional hazards analyses adjusted for sociodemographic and clinical factors.
For HL, the adjusted risk for death for Medicaid enrolled compared with nonenrolled patients was 1.98 (95% confidence interval [CI], 1.47–2.68) in NY and 1.89 (95% CI, 1.43–2.49) in CA. In contrast, for AML, Medicaid enrollment had no effect on survival (adjusted hazard ratio, 1.00; 95% CI, 0.84–1.19 in NY and hazard ratio, 1.02; 95% CI, 0.89–1.16 in CA). These results persisted despite adjusting for race/ethnicity and other factors.
Poverty does not affect survival for AML patients but does appear to be associated with survival for HL patients, who, in contrast to AML patients, require complex outpatient treatment. Challenges for the poor in adhering to treatment regimens for HL could explain this disparity and merit further study.
PMCID: PMC3228153  PMID: 21873583
Health care disparities; Medicaid; Socioeconomic factors; Neoplasms; Hodgkin's disease; Acute myeloid leukemia
13.  Reproductive Factors and Non-Hodgkin Lymphoma Risk in the California Teachers Study 
PLoS ONE  2009;4(12):e8135.
Non-Hodgkin lymphoma (NHL) is a malignancy etiologically linked to immunomodulatory exposures and disorders. Endogenous female sex hormones may modify immune function and influence NHL risk. Few studies have examined associations between reproductive factors, which can serve as surrogates for such hormonal exposures, and NHL risk by subtype.
Methodology/Principal Findings
Women in the California Teachers Study cohort provided detailed data in 1995–1996 on reproductive history. Follow-up through 2007 identified 574 women with incident B-cell NHL. Hazard rate ratios (RR) and 95% confidence intervals (CI) were estimated using Cox proportional hazards models to assess associations between reproductive factors and all B-cell NHL combined, diffuse large B-cell lymphomas, follicular lymphomas, and B-cell chronic lymphocytic leukemias/small lymphocytic lymphomas. Pregnancy was marginally associated with lower risk of B-cell NHL (RR = 0.84, 95% CI = 0.68–1.04). Much of the reduction in risk was observed after one full-term pregnancy relative to nulligravid women (RR = 0.75, 95% CI = 0.54–1.06; P for trend <0.01), particularly for diffuse large B-cell lymphomas (P for trend = 0.13), but not among women who had only incomplete pregnancies. Age at first full-term pregnancy was marginally inversely associated with B-cell NHL risk overall (P for trend = 0.08) and for diffuse large B-cell lymphomas (P for trend = 0.056). Breast feeding was not associated with B-cell NHL risk overall or by subtype.
Full-term pregnancy and early age at first full-term pregnancy account for most of the observed reduction in B-cell NHL risk associated with gravidity. Pregnancy-related hormonal exposures, including prolonged and high-level exposure to progesterone during a full-term pregnancy may inhibit development of B-cell NHL.
PMCID: PMC2780313  PMID: 19956586
14.  Advanced paternal age increases the risk of schizophrenia and obsessive–compulsive disorder in a Chinese Han population 
Psychiatry Research  2012;198(3):353-359.
Using the Structured Clinical Interview for DSM-IV, patient and non-patient version (SCID-P/NP), this study investigated 351 patients with schizophrenia, 122 with obsessive–compulsive disorder (OCD), and 238 unrelated healthy volunteers in a Chinese Han population. The relative risks posed by advanced paternal age for schizophrenia and OCD in offspring were computed under logistic regression analyses and adjusted for the participant's sex, age and co-parent age at birth. Compared to the offspring with paternal age of 25–29 years old, the relative risks rose from 2.660 to 10.183 in the paternal age range of 30–34 and ≥ 35. The relative risks for OCD increased from 2.225 to 5.413 in 30–34 and ≥ 35. For offspring with paternal age of < 25, the odds ratios of developing schizophrenia and OCD were 0.628 and 0.289 respectively, whereas an association between increased maternal age and risk for schizophrenia/OCD was not seen. Interaction analysis showed an interaction effect between paternal age and maternal age at birth. Such a tendency of risk affected by parental age for schizophrenia and OCD existed after splitting out the data of early onset patients. Sex-specific analyses found that the relative risks for schizophrenia with paternal age of 30–34 and ≥ 35 in male offspring were 2.407 and 10.893, and in female offspring were 3.080 and 9.659. The relative risks for OCD with paternal age of 30–34 and ≥ 35 in male offspring were 3.493 and 7.373, and in female offspring 2.005 and 4.404. The mean paternal age of schizophrenia/OCD patients born before the early 1980s was much greater than that of patients who were born after then. The findings illustrated that advanced paternal age is associated with increased risk for both schizophrenia and OCD in a Chinese Han population, prominently when paternal age is over 35. Biological and non-biological mechanisms may both be involved in the effects of advanced paternal age on schizophrenia and OCD.
PMCID: PMC3778893  PMID: 22424906
Paternal age; Schizophrenia; Obsessive–compulsive disorder; Chinese population
15.  Dietary phytocompounds and risk of lymphoid malignancies in the California Teachers Study cohort 
Cancer causes & control : CCC  2010;22(2):237-249.
We examined whether dietary intake of isoflavones, lignans, isothiocyanates, antioxidants, or specific foods rich in these compounds is associated with reduced risk of B-cell non-Hodgkin lymphoma (NHL), multiple myeloma (MM), or Hodgkin lymphoma (HL) in a large, prospective cohort of women.
Between 1995-1996 and December 31, 2007, among 110,215 eligible members of the California Teachers Study cohort, 536 women developed incident B-cell NHL, 104 developed MM, and 34 developed HL. Cox proportional hazards regression, with age as the time-scale, was used to estimate adjusted rate ratios (RRs) with 95% confidence intervals (CIs) for risk of lymphoid malignancies.
Weak inverse associations with risk of diffuse large B-cell lymphoma were observed for isothiocyanates (RR for ≥12.1 vs. <2.7 mcM/day=0.67, 95% CI: 0.43-1.05) and an antioxidant index measuring hydroxyl radical absorbance capacity (RR for ≥2.2 vs. <0.9 μM Trolox equiv/g/day=0.68, 95% CI: 0.42-1.10; ptrend=0.08). Risk of other NHL subtypes, overall B-cell NHL, MM, or HL was not generally associated with dietary intake of isoflavones, lignans, isothiocyanates, antioxidants, or major food sources of these compounds.
Isoflavones, lignans, isothiocyanates, and antioxidant compounds are not associated with risk of most B-cell malignancies, but some phytocompounds may decrease risk of selected subtypes.
PMCID: PMC3074494  PMID: 21107674
lymphoma; diet; isothiocyanates; antioxidants; cohort studies
16.  Mortality From Lymphohematopoietic Malignancies Among Workers in Formaldehyde Industries: The National Cancer Institute Cohort 
Formaldehyde exposure is associated with leukemia in some epidemiological studies. In the National Cancer Institute’s formaldehyde cohort, previously followed through December 31, 1979, and updated through December 31, 1994, formaldehyde exposure was associated with an increased risk for leukemia, particularly myeloid leukemia, that increased with peak and average intensity of exposure.
We extended follow-up through December 31, 2004 (median follow-up = 42 years), for 25 619 workers employed at one of 10 formaldehyde-using or formaldehyde-producing plants before 1966. We used Poisson regression to calculate relative risk (RR) estimates and 95% confidence intervals (CIs) to examine associations between quantitative formaldehyde exposure estimates (peak exposure, average intensity and cumulative exposure) and death from lymphohematopoietic malignancies. All statistical tests were two-sided and considered to be significant at P = .05.
When follow-up ended in 2004, there were statistically significant increased risks for the highest vs lowest peak formaldehyde exposure category (≥4 parts per million [ppm] vs >0 to <2.0 ppm) and all lymphohematopoietic malignancies (RR = 1.37; 95% CI = 1.03 to 1.81, P trend = .02) and Hodgkin lymphoma (RR = 3.96; 95% CI = 1.31 to 12.02, P trend = .01). Statistically nonsignificant associations were observed for multiple myeloma (RR = 2.04; 95% CI = 1.01 to 4.12, P trend > .50), all leukemia (RR = 1.42; 95% CI = 0.92 to 2.18, P trend = .12), and myeloid leukemia (RR = 1.78; 95% CI = 0.87 to 3.64, P trend = .13). There was little evidence of association for any lymphohematopoietic malignancy with average intensity or cumulative exposure at the end of follow-up in 2004. However, disease associations varied over time. For peak exposure, the highest formaldehyde-related risks for myeloid leukemia occurred before 1980, but trend tests attained statistical significance in 1990 only. After the mid-1990s, the formaldehyde-related risk of myeloid leukemia declined.
Evaluation of risks over time suggests a possible link between formaldehyde exposure and lymphohematopoietic malignancies, particularly myeloid leukemia but also perhaps Hodgkin lymphoma and multiple myeloma. Observed patterns could be due to chance but are also consistent with a causal association within the relatively short induction–incubation periods characteristic of leukemogenesis. Further epidemiological study and exploration of potential molecular mechanisms are warranted.
PMCID: PMC2684555  PMID: 19436030
17.  Allergic conditions and risk of hematological malignancies in adults: a cohort study 
BMC Public Health  2004;4:51.
Two contradictory hypotheses have been proposed to explain the relationship between allergic conditions and malignancies, the immune surveillance hypothesis and the antigenic stimulation hypothesis. The former advocates that allergic conditions may be protective against development of cancer, whereas the latter proposes an increased risk. This relationship has been studied in several case-control studies, but only in a few cohort studies.
The association between allergic conditions and risk of developing leukemia, Hodgkin's disease, non-Hodgkin's lymphoma and myeloma was investigated in a cohort of 16,539 Swedish twins born 1886–1925. Prospectively collected, self-reported information about allergic conditions such as asthma, hay fever or eczema was obtained through questionnaires administered in 1967. The cohort was followed 1969–99 and cancer incidence was ascertained from the Swedish Cancer Registry.
Hives and asthma tended to increase the risk of leukemia (relative risk [RR] = 2.1, 95% Confidence Interval [CI] 1.0–4.5 and RR = 1.6, 95% CI 0.8–3.5, respectively). There was also an indication of an increased risk of non-Hodgkin's lymphoma associated with eczema during childhood (RR = 2.3, 95% CI 1.0–5.3).
In contrast to most previous studies, our results do not indicate a protective effect of allergic conditions on the risk of developing hematological malignancies. Rather, they suggest that allergic conditions might increase the risk of some hematological malignancies.
PMCID: PMC534807  PMID: 15527506
18.  Increased Risk for Lymphoid and Myeloid Neoplasms in Elderly Solid Organ Transplant Recipients 
By assessing the spectrum of hematologic malignancies associated with solid organ transplantation in the elderly, we provide information on the pathogenesis of lymphoid and myeloid neoplasms and the clinical manifestations of immunosuppression.
Using data from the U.S. Surveillance, Epidemiology, and End Results (SEER) Medicare database, we identified 83,016 cases with a hematologic malignancy (age 66-99 years) and 166,057 population-based controls matched to cases by age, sex, and calendar year. Medicare claims were used to identify a history of solid organ transplantation. We utilized polytomous logistic regression to calculate odds ratios (ORs) comparing transplantation history among cases with various hematologic malignancy subtypes and controls, adjusting for the matching factors and race.
A prior solid organ transplant was identified in 216 (0.26%) cases and 204 (0.12%) controls. Transplantation was associated with increased risk for non-Hodgkin lymphomas (NHLs) (OR=2.13, 95%CI 1.67-2.72), especially diffuse large B-cell lymphoma (OR=3.29, 95%CI 2.28-4.76), marginal zone lymphoma (OR=2.48, 95%CI 1.17-5.22), lymphoplasmacytic lymphoma (OR=3.32, 95%CI 1.41-7.81), and T-cell lymphoma (OR=3.07, 95%CI 1.56-6.06). Transplantation was also associated with elevated risk of Hodgkin lymphoma (OR=2.53, 95%CI 1.01-6.35) and plasma cell neoplasms (OR=1.91, 95%CI 1.24-2.93). Risks for myeloid neoplasms were also elevated (OR=1.99, 95%CI 1.41-2.81).
Solid organ transplantation is associated with a wide spectrum of hematologic malignancies in the elderly. Risk was increased for four specific NHL subtypes for which a viral agent has been implicated, supporting an added role for immunosuppression.
Our results support monitoring for a wide spectrum of hematologic malignancies following solid organ transplant.
PMCID: PMC2866098  PMID: 20406959
transplantation; lymphoma; myeloma; leukemia; United States
19.  Perinatal and Family Risk Factors for Hodgkin Lymphoma in Childhood Through Young Adulthood 
American Journal of Epidemiology  2012;176(12):1147-1158.
The incidence of Hodgkin lymphoma has increased among adolescents and young adults in recent decades, but the relevant risk factors in early life are still unknown. A national cohort study was conducted of 3,571,574 individuals born in Sweden in 1973–2008 and followed up for Hodgkin lymphoma incidence through 2009, to examine perinatal and family risk factors for Hodgkin lymphoma in childhood through young adulthood (ages 0–37 years). There were 943 Hodgkin lymphoma cases identified in 66.3 million person-years of follow-up. High fetal growth was associated with an increased risk of Hodgkin lymphoma after adjustment for gestational age at birth and other potential confounders (Ptrend = 0.005). Family history of Hodgkin lymphoma in a sibling or parent also was strongly associated with an increased risk, with adjusted hazard ratios = 8.83 (95% confidence interval: 3.67, 21.30) and 7.19 (95% confidence interval: 3.58, 14.44), respectively. No association was found between gestational age at birth, birth order, twinning, parental age, or parental education and Hodgkin lymphoma. These findings did not vary by age at Hodgkin lymphoma diagnosis. Similar associations were found for nodular sclerosis and mixed cellularity subtypes. These findings suggest that perinatal factors including possible growth factor pathways may contribute to the risk of Hodgkin lymphoma in childhood through young adulthood.
PMCID: PMC3571233  PMID: 23171883
birth order; family; fetal development; gestational age; Hodgkin disease; lymphoma; maternal age
20.  Estimated Autism Risk and Older Reproductive Age 
American journal of public health  2009;99(9):1673-1679.
We sought to estimate the risk for autism associated with maternal and paternal age across successive birth cohorts.
We linked birth records and autism diagnostic records from the California Department of Developmental Services for children born in California between 1992 and 2000 to calculate the risk associated with maternal and paternal age for each birth cohort as well as for the pooled data.
The categorical risks associated with maternal age over 40 years ranged from a high of 1.84 (95% confidence interval [CI]=1.37, 2.47) to a low of 1.27 (95% CI=0.95, 1.69). The risk associated with paternal age ranged from 1.29 (95% CI=1.03, 1.6) to 1.71 (95% CI=1.41, 2.08).
Pooling data across multiple birth cohorts inflates the risk associated with paternal age. Analyses that do not suffer from problems produced by pooling across birth cohorts demonstrated that advanced maternal age, rather than paternal age, may pose greater risk. Future research examining parental age as a risk factor must be careful to avoid the paradoxes that can arise from pooling data, particularly during periods of social demographic change.
PMCID: PMC2724463  PMID: 19608957
21.  Correlations of hematological parameters with bone marrow findings in chronic lymphoproliferative disorders associated with hepatitis viruses 
Journal of Medicine and Life  2013;6(4):464-471.
Background. Hepatitis B and C viruses’ infections are often associated with hematological disorders in evolution, suggesting that these viruses have a tropism for peripheral blood and/or bone marrow cells.
Aim. To analyze the hematological parameters and bone marrow findings in a group of patients diagnosed with chronic lymphoproliferative disorders (CLD) and hepatitis viruses B, C, D infections, which were included in the research grant (acronym LIMFO-VIR) between December 2007 and May 2010 in the Hematology Department of the Emergency University Hospital of Bucharest.
Methods and results. Patients were diagnosed by using immunopathology according to the WHO criteria. The analyzed group included 42 patients (both sexes), with the mean age of 60,35 years. The most frequent hematologic disease was non-Hodgkin’s lymphoma 30/42 (71,42%), followed by chronic lymphocytic leukemia (16,66%) and Hodgkin’s lymphoma (7,14%). Hepatitis viruses were distributed: 17/42 (40,47%) patients with HBV, 22/42 (52,38%) with HCV and 3/42 (7,14%) had a double/triple association of viruses. Most of the patients had an indolent type of disease - 27/42 (64,28%), whereas 15/42 (35,71%) had an aggressive one, pattern found both in the HBV and HCV infected groups. An abnormal bone marrow result was revealed in 32/42 (76,19%) patients, 19 (59,37%) of them being HCV infected. Myelodysplasia was found in 6/42(14,28%) patients, the majority being HCV infected, all having an indolent form of CLD. The antiviral therapy did not influence the hematological parameters (no significant differences were found between the groups with/without an antiviral therapy).
Discussions. Patients with hepatitis virus infections may associate neutropenia and thrombocytopenia; the mechanisms are thought to involve hypersplenism, autoimmune processes and antiviral therapy. We excluded the influence of chemotherapy, as the study was performed before the treatment. In our group, patients whether HBV or HCV infected, presented an isolated cytopenia. The abnormal bone marrow cellularity (increased or decreased) and dysplasia were found especially in the HCV group. There are studies showing no association between myelodysplasia and hepatitis viruses; others found a strong relation of these. One of the mechanisms of myelodysplasia could be a dysregulation of the immune system.
Conclusions. Bone marrow/peripheral blood features correlate with the type of viral infection and HCV is more prone to develop additional hematological changes than HBV. The degree of bone marrow involvement by CLDs influences these features. We considered mandatory to perform a bone marrow analysis at the diagnosis of CLDs to stage and to establish if other bone marrow changes were present, a crucial aspect for therapy and outcome of the disease. The association between the hepatitis viruses – myelodysplasia- autoimmunity seems to have a role in the lymphoproliferative disorders etiology.
Abbreviations: CLD – chronic lymphoproliferative disorders; NHL- non-Hodgkin’s lymphoma, CLL- chronic lymphocytic leukemia, HL- Hodgkin’s lymphoma, MDS – myelodysplastic syndrome, AML – acute myeloid leukemia
PMCID: PMC4034312  PMID: 24868264
hepatitis viruses; chronic lymphoproliferative disorders; myelodysplasia; cytopenia
22.  Cohort study of non-Hodgkin lymphoma risk in association with hepatitis B virus infection in South Korea 
The lancet oncology  2010;11(9):827-834.
Hepatitis B virus (HBV) infection is common throughout Asia and Africa. Evidence is inconclusive regarding whether chronic HBV infection increases risk for non-Hodgkin lymphoma (NHL).
We conducted a cohort study of 603,585 South Korean workers and their dependents enrolled during 1992–1995. Serum hepatitis B surface antigen (HBsAg) measured at baseline indicated the presence of chronic HBV infection. We ascertained hematologic malignancies using national inpatient, outpatient, and mortality databases through 2006. Cox regression was used to evaluate associations with HBsAg status, adjusting for sex, age, and enrollment year.
53,045 subjects (8.8%) were HBsAg positive at baseline. Subsequently, 133 HBsAg positive and 905 HBsAg negative individuals developed NHL. HBsAg positive subjects had elevated risk of NHL overall (incidence 19.4 vs. 12.3 per 100,000 person-years; adjusted hazard ratio [HR] 1.74, 95%CI 1.45–2.09). Among NHL subtypes, risk was significantly elevated in association with HBsAg positivity for diffuse large B cell lymphoma (N=325 cases; adjusted HR 2.01, 95%CI 1.48–2.75) and non-significantly elevated for follicular NHL (N=47; 1.67, 0.71–3.95) and T-cell NHL (N=75; 1.40, 0.67–2.92); risk was also elevated for other/unknown NHL subtypes (N=591; 1.65, 1.29–2.11). Elevated risk was also observed for malignant immunoproliferation (N=14; adjusted HR 3.79, 95%CI, 1.05–13.7), a category that includes Waldenström macroglobulinemia. Risk of these malignancies was consistently elevated in HBsAg positive subjects throughout 14 years of follow-up. HBsAg positivity was not associated with Hodgkin lymphoma, multiple myeloma, or various leukemias.
During extended follow-up, HBsAg positive individuals manifested an elevated risk of NHL, suggesting that chronic infection promotes lymphomagenesis.
PMCID: PMC2933963  PMID: 20688564
23.  Birth characteristics and the risk of childhood leukaemias and lymphomas in New Zealand: a case-control study 
Some studies have found that lower parity and higher or lower social class (depending on the study) are associated with increased risks of childhood acute lymphoblastic leukaemia (ALL). Such findings have led to suggestions that infection could play a role in the causation of this disease. An earlier New Zealand study found a protective effect of parental marriage on the risk of childhood ALL, and studies elsewhere have reported increased risks in relation to older parental ages. This study aimed to assess whether lower parity, lower social class, unmarried status and older parental ages increase the risk of childhood ALL (primarily). These variables were also assessed in relation to the risks of childhood acute non-lymphoblastic leukaemia, non-Hodgkin's lymphomas and Hodgkin's disease.
A case control study was conducted. The cases were 585 children diagnosed with leukaemias or lymphomas throughout New Zealand over a 12 year period. The 585 age and sex matched controls were selected at random from birth records. Birth records from cases (via cancer registration record linkage) and from controls provided accurate data on maternal parity, social class derived from paternal occupation, maternal marital status, ages of both parents, and urban status based on the address on the birth certificate. Analysis was by conditional logistic regression.
There were no statistically significant associations overall between childhood ALL and parity of the mother, social class, unmarried maternal status, increasing parental ages (continuous analysis), or urban status. We also found no statistically significant associations between the risks of childhood acute non-lymphoblastic leukaemia, non-Hodgkin lymphomas, or Hodgkin's disease and the variables studied.
This study showed no positive results though of reasonable size, and its record linkage design minimised bias. Descriptive studies (eg of time trends of ALL) show that environmental factors must be important for some diagnoses. Work has been done on the risk of ALL in relation to chemicals (eg pesticides) and drugs, dietary factors (eg vitamins), electromagnetic fields and infectious hypotheses (to name some); but whether these or other unknown factors are truly important remains to be seen.
PMCID: PMC1592292  PMID: 16972984
24.  Regular recreational physical activity and risk of hematologic malignancies: results from the prospective VITamins And lifestyle (VITAL) study† 
Annals of Oncology  2012;24(5):1370-1377.
Conflicting evidence exists on the relationship between physical activity (PA) and incident hematologic malignancies. Herein, we used a large cohort study to examine this association.
Patients and methods
Sixty-five thousand three hundred twenty-two volunteers aged 50–76 years were recruited from 2000 to 2002. Incident hematologic malignancies (n = 666) were identified through 2009 by linkage to the Surveillance, Epidemiology, and End Results cancer registry. Hazard ratios (HRs) for hematologic malignancies associated with PA averaged over 10 years before baseline were estimated with Cox proportional hazards models, adjusting for factors associated with hematologic cancers or PA.
There was a decreased risk of hematologic malignancies associated with PA (HR = 0.66 [95% confidence interval, 95% CI 0.51–0.86] for the highest tertile of all PA, P-trend = 0.005, and HR = 0.60 [95% CI 0.44–0.82] for the highest tertile of moderate/high-intensity PA, P-trend = 0.002). These associations were strongest for myeloid neoplasms (HR = 0.48 [95% CI 0.29–0.79] for the highest tertile of all PA, P-trend = 0.013, and HR = 0.40 [95% CI 0.21–0.77] for the highest tertile of moderate/high-intensity PA, P-trend = 0.016). There were also significant associations between PA and chronic lymphocytic leukemia/small lymphocytic lymphoma or other mature B-cell lymphomas except plasma cell disorders.
Our study offers the strongest epidemiological evidence, to date, to suggest an association between regular PA and dose-dependent risk reduction for most hematologic malignancies, particularly myeloid neoplasms.
PMCID: PMC3629898  PMID: 23247659
cancer risk; epidemiology; hematologic malignancies; physical activity; prospective cohort study; VITamins And Lifestyle study
25.  Advanced Parental Age and the Risk of Autism Spectrum Disorder 
American Journal of Epidemiology  2008;168(11):1268-1276.
This study evaluated independent effects of maternal and paternal age on risk of autism spectrum disorder. A case-cohort design was implemented using data from 10 US study sites participating in the Centers for Disease Control and Prevention's Autism and Developmental Disabilities Monitoring Network. The 1994 birth cohort included 253,347 study-site births with complete parental age information. Cases included 1,251 children aged 8 years with complete parental age information from the same birth cohort and identified as having an autism spectrum disorder based on Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision criteria. After adjustment for the other parent's age, birth order, maternal education, and other covariates, both maternal and paternal age were independently associated with autism (adjusted odds ratio for maternal age ≥35 vs. 25–29 years = 1.3, 95% confidence interval: 1.1, 1.6; adjusted odds ratio for paternal age ≥40 years vs. 25–29 years = 1.4, 95% confidence interval: 1.1, 1.8). Firstborn offspring of 2 older parents were 3 times more likely to develop autism than were third- or later-born offspring of mothers aged 20–34 years and fathers aged <40 years (odds ratio = 3.1, 95% confidence interval: 2.0, 4.7). The increase in autism risk with both maternal and paternal age has potential implications for public health planning and investigations of autism etiology.
PMCID: PMC2638544  PMID: 18945690
autistic disorder; birth order; maternal age; paternal age

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