David J. Tollerud

Familial testicular cancer and urogenital developmental anomalies.

In a case‐control study of testicular cancer, 6 of 269 cases (2.2%) reported a first‐degree relative with testicular cancer, compared to 1 of 259 controls (0.4%). Fathers and brothers of testicular cancer cases had a six‐fold elevated risk of developing a testicular malignancy compared to men in the general population. Cryptorchidism was reported in a first‐degree relative in 1 (17%) of the familial cases versus 7 of 259 (2.7%) controls and 14 of 263 (5.3%) cases with a negative family history for testicular cancer. One half of the 6 familial cases reported a first‐degree relative with a groin hernia (all surgically repaired before age 12), compared to 12.7% of 259 controls and 10.3% of 263 nonfamilial cases. Three familial clusters identified through the case‐control study were selected for clinical evaluation. One of the 6 surviving males with testicular cancer in these 3 families had undergone orchiopexy and inguinal herniorrhaphy at age 6 years, and one had a hydrocele associated with his testicular tumor. Of the 12 living fathers and brothers of these 6 men, 3 reported childhood inguinal hernias, two with coexisting hydroceles. One additional hernia and two additional hydroceles were detected during urologic evaluation of these healthy relatives. The high prevalence of cryptorchidism, inguinal hernias, and hydroceles among men in these families suggests that an underlying alteration in urogenital embryogenesis may be associated with the familial predisposition to testicular neoplasia.

T-cell subsets in healthy teenagers: Transition to the adult phenotype☆

Little is known about the normal range and variability of T-cell subsets in older children. We analyzed peripheral blood mononuclear cell subsets in 112 healthy children, ages 12-19 years (mean +/- SD: 15.4 +/- 1.9 years), using monoclonal antibodies and flow cytometry. The study population included 28 blacks and 84 whites, with 59 boys and 53 girls. The mean +/- SD cell subset values were: CD3+ T cells, 74.0 +/- 7.8%; CD4+ helper-inducer T cells, 46.8 +/- 6.9%; CD8+ suppressor-cytotoxic T cells, 27.3 +/- 5.7%; CD4:CD8 helper:suppressor ratio, 1.81 +/- 0.57; CD16+ natural killer cells, 4.4 +/- 3.1%; CD19+ B cells, 10.0 +/- 5.3%; CD14+ monocytes, 20.0 +/- 6.5%; and HLA-DR cells, 15.4 +/- 4.8%. Overall, boys had a higher proportion of HLA-DR+ cells than girls, attributable to an increase in CD19+ B cells. Blacks tended to have a higher proportion of HLA-DR+ cells than whites, apparently due to an increase in activated T cells. Detailed analysis by age group revealed a striking transition in the pattern of CD4+ and CD8+ cell populations. The CD4:CD8 ratio, higher in boys than girls for ages 12-16, was reversed to the adult pattern in 17-19 year olds, with a higher CD4:CD8 ratio in girls. These data provide important baseline values for healthy children and stress the importance of establishing normative ranges for pediatric subjects separately from adults.

The Health Effects of Automobile Exhaust. VI. Relationship of Respiratory Symptoms and Pulmonary Function in Tunnel and Turnpike Workers

To examine the effect of automobile exhaust on respiratory symptoms and pulmonary function, the authors studied 175 tunnel and turnpike workers employed by the Massachusetts Turnpike Authority on two occasions 3 yr apart beginning in 1972. A standard respiratory symptom and illness questionnaire was administered, spirometry was performed, and proximal hair lead and blood lead content were measured as biologic indices of automobile exhaust exposure. One hundred nine (63%) workers were current cigarette smokers, 41 (23%) were exsmokers, and 24 (14%) had never smoked. Smoking was strongly related to respiratory symptoms of cough (P less than .001) and phlegm production (P less than .001), but not to wheezing (P = .41), breathlessness (P = .14), bronchial asthma (P = .13), or frequent chest colds (P = .14). When workers were stratified by smoking status, no effect could be seen between high automobile exhaust exposure as measured by a variety of parameters and all of the above respiratory symptoms and illnesses. The level of pulmonary function [forced expiratory volume in 1 sec (FEV1.0) and forced vital capacity (FVC)] was not related to past or current exhaust exposure in a cross-sectional analysis when we controlled for age, height, and cigarette consumption. In a prospective analysis of 84 of these workers, the observed changes in FEV1.0 and FVC over 3 yr were unrelated to exhaust exposure after controlling for age, height, cigarette consumption, and initial level of pulmonary function.