1082
Cervical smears per 1000 Wales and Scotland.
Year aged 15-64 in England and
women
reaped by the mid-1980s? The screening plateau in 1975-82 can be seen in all health regions. Possible explanations may lie in the decline in the birth rate to a trough in 1977 (meaning fewer antenatal visits and smears) and in the fears aroused at the same time by publicity about the link between oral contraceptives and cardiovascular disease, leading many women to stop using this form of birth control thus reducing opportunist smear taking during consultations about the prescription of oral
contraceptives.3 We know that even infrequent smear taking (say every 10 years) for all women confers substantial protection.’ So perhaps the combination of the screening programme and opportunistic screening in diverse settings, albeit a patchwork effort at a level below the rate equivalent to one woman every five years, was more effective than the sceptics believed.5,6 If so, prospects for the 1990s may be quite bright, even in Britain. Department of Public Health and Primary Health Care, University of Oxford, Gibson Laboratories Building, Radcliffe Infirmary, Oxford OX2 6HE, UK
MIKE MURPHY RUAIRIDH MILNE
Murphy M, Osmond C. Predicting mortality from cancer of the uterine cervix from Commun Health (in press). 1991-2001. Epidemiol J 2. Beral V, Booth M. Predictions of cervical cancer incidence and mortality in England 1.
and Wales. Lancet 1986; i: 818. 3. Bone M. Family planning in Scotland in 1982: a survey carried out on behalf of the Scottish Home and Health Department by the Office of Population Censuses and Surveys Social Survey Division. London: HM Stationery Office, 1985. 4. Hakama M, Miller AB,Day NE, eds. Screening for cancer of the uterine cervix (IARC Publ no 76). Lyon: IARC, 1986. 5. Editorial. Cancer of the cervix: death by incompetence. Lancet 1985; ii: 363-64. 6. Murphy MFG, Cambell MJ, Goldblatt PO. Twenty years screening for cancer of the uterine cervix in Great Britain 1964-84; further evidence for its ineffectiveness. J Epidemiol Commun Health 1988; 42: 49-53.
Parental occupation and risk of prematurity SIR,-Dr Sanjose and colleagues (Aug 17, p 428) conclude that
parental occupational exposures do not have a profound effect on the risk of prematurity. They also suggest that if there is any adverse effect it is associated with maternal rather than paternal exposures. We feel that these conclusions are somewhat overstated, especially in view of the potential misclassification inherent in relying on job titles as a surrogate for exposure, and in the absence of data on cigarette smoking, an important potential confounder that is quite possibly related to both occupation and adverse pregnancy outcome.
Despite these limitations, Sanjose and colleagues’ report of a 1 9-fold increased risk of preterm delivery among the offspring of male ceramics workers is consistent with our earlier finding from the US National Natality Survey (NNS) of increased risk associated with paternal employment in the glass, clay, and stone industry (odds ratio 23,95% confidence interval 0.8-6.3).1 Workers in this industry are potentially exposed to reproductive hazards such as lead and benzene, which may affect fetal development through genetic alteration of the spermatozoa or though contamination of the home environment.2 Our observation of a 2-fold increased risk of preterm delivery among offspring of male workers in the textile industry was also corroborated, to a lesser extent, by Sanjose et al (RR 1-3). Both these occupational groups were associated with increases in small-for-gestational-age deliveries in the USA and in Scotland. Rather than discouraging further study of parental occupational exposures, Sanjose and colleagues’ findings suggest the need for more rigorous evaluation of such effects in epidemiological studies. Exploratory analyses such as this are useful to identify broad categories of exposures that deserve further examination, especially with a systematic evaluation of relevant publications. However, the inherent quality of the exposure data makes such studies incapable of exonerating potentially hazardous exposures. Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina 27599, USA
E. A. WHELAN D. A. SAVITZ
1. Savitz
DA, Whelan EA, Kleckner RC. Effect of parents’ occupational exposures on risk of stillbirth, preterm delivery, and small-for-gestational-age infants. AmJ Epidemiol 1989; 129: 1201-18. 2. Knishkowy B, Baker EL. Transmission of occupational disease to family members. Am J Ind Med 1986; 9: 545-50.
Biopsy-proven myositis with microvasculitis in association with carbimazole SIR,-Only 3 cases of myositis associated with carbimazole therapy have been reported,! but muscle biopsy was not done in any of these. We present a biopsy-proven case of carbimazole-related myositis. A 36-year-old woman from Laos was referred to our department in January, 1991, for evaluation of congestive heart failure with atrial fibrillation and weight loss of 7 kg in 10 months. Her history was unremarkable. She had signs of congestive heart failure, firm cervical lymphadenopathies, an enlarged thyroid gland, and exophthalmos. She had no muscle pain and strength testing was normal.
Graves’ disease was confirmed (thyroid stimulating hormone [TSH]
Cervical smears per 1000 Wales and Scotland.
Year aged 15-64 in England and
women
reaped by the mid-1980s? The screening plateau in 1975-82 can be seen in all health regions. Possible explanations may lie in the decline in the birth rate to a trough in 1977 (meaning fewer antenatal visits and smears) and in the fears aroused at the same time by publicity about the link between oral contraceptives and cardiovascular disease, leading many women to stop using this form of birth control thus reducing opportunist smear taking during consultations about the prescription of oral
contraceptives.3 We know that even infrequent smear taking (say every 10 years) for all women confers substantial protection.’ So perhaps the combination of the screening programme and opportunistic screening in diverse settings, albeit a patchwork effort at a level below the rate equivalent to one woman every five years, was more effective than the sceptics believed.5,6 If so, prospects for the 1990s may be quite bright, even in Britain. Department of Public Health and Primary Health Care, University of Oxford, Gibson Laboratories Building, Radcliffe Infirmary, Oxford OX2 6HE, UK
MIKE MURPHY RUAIRIDH MILNE
Murphy M, Osmond C. Predicting mortality from cancer of the uterine cervix from Commun Health (in press). 1991-2001. Epidemiol J 2. Beral V, Booth M. Predictions of cervical cancer incidence and mortality in England 1.
and Wales. Lancet 1986; i: 818. 3. Bone M. Family planning in Scotland in 1982: a survey carried out on behalf of the Scottish Home and Health Department by the Office of Population Censuses and Surveys Social Survey Division. London: HM Stationery Office, 1985. 4. Hakama M, Miller AB,Day NE, eds. Screening for cancer of the uterine cervix (IARC Publ no 76). Lyon: IARC, 1986. 5. Editorial. Cancer of the cervix: death by incompetence. Lancet 1985; ii: 363-64. 6. Murphy MFG, Cambell MJ, Goldblatt PO. Twenty years screening for cancer of the uterine cervix in Great Britain 1964-84; further evidence for its ineffectiveness. J Epidemiol Commun Health 1988; 42: 49-53.
Parental occupation and risk of prematurity SIR,-Dr Sanjose and colleagues (Aug 17, p 428) conclude that
parental occupational exposures do not have a profound effect on the risk of prematurity. They also suggest that if there is any adverse effect it is associated with maternal rather than paternal exposures. We feel that these conclusions are somewhat overstated, especially in view of the potential misclassification inherent in relying on job titles as a surrogate for exposure, and in the absence of data on cigarette smoking, an important potential confounder that is quite possibly related to both occupation and adverse pregnancy outcome.
Despite these limitations, Sanjose and colleagues’ report of a 1 9-fold increased risk of preterm delivery among the offspring of male ceramics workers is consistent with our earlier finding from the US National Natality Survey (NNS) of increased risk associated with paternal employment in the glass, clay, and stone industry (odds ratio 23,95% confidence interval 0.8-6.3).1 Workers in this industry are potentially exposed to reproductive hazards such as lead and benzene, which may affect fetal development through genetic alteration of the spermatozoa or though contamination of the home environment.2 Our observation of a 2-fold increased risk of preterm delivery among offspring of male workers in the textile industry was also corroborated, to a lesser extent, by Sanjose et al (RR 1-3). Both these occupational groups were associated with increases in small-for-gestational-age deliveries in the USA and in Scotland. Rather than discouraging further study of parental occupational exposures, Sanjose and colleagues’ findings suggest the need for more rigorous evaluation of such effects in epidemiological studies. Exploratory analyses such as this are useful to identify broad categories of exposures that deserve further examination, especially with a systematic evaluation of relevant publications. However, the inherent quality of the exposure data makes such studies incapable of exonerating potentially hazardous exposures. Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina 27599, USA
E. A. WHELAN D. A. SAVITZ
1. Savitz
DA, Whelan EA, Kleckner RC. Effect of parents’ occupational exposures on risk of stillbirth, preterm delivery, and small-for-gestational-age infants. AmJ Epidemiol 1989; 129: 1201-18. 2. Knishkowy B, Baker EL. Transmission of occupational disease to family members. Am J Ind Med 1986; 9: 545-50.
Biopsy-proven myositis with microvasculitis in association with carbimazole SIR,-Only 3 cases of myositis associated with carbimazole therapy have been reported,! but muscle biopsy was not done in any of these. We present a biopsy-proven case of carbimazole-related myositis. A 36-year-old woman from Laos was referred to our department in January, 1991, for evaluation of congestive heart failure with atrial fibrillation and weight loss of 7 kg in 10 months. Her history was unremarkable. She had signs of congestive heart failure, firm cervical lymphadenopathies, an enlarged thyroid gland, and exophthalmos. She had no muscle pain and strength testing was normal.
Graves’ disease was confirmed (thyroid stimulating hormone [TSH]
