BMJ No 7114 Volume 315 This week in brief Saturday 18 October 1997
Exposure to environmental tobacco smoke increases risk of
ischaemic heart disease and lung cancer
Moderately decreased sperm count is not a risk for testicular
cancer
Bedside test for paracetamol poisoning gives inconsistent results
Smoker's paradox goes up in smoke
Treating the obesity epidemic
Exposure to environmental tobacco smoke increases risk of
ischaemic heart disease and lung cancer
Two papers from Wald and colleagues examine the health effects of
environmental tobacco smoke. On page 973 Law et al seek to explain why
the excess risk of ischaemic heart disease in non-smokers who live with
smokers (30%) is so large when smokers themselves have only 2-3 times
that risk. Part of the explanation is due to dietary differences
between non-smokers who live with smokers and those who live with
non-smokers, but most of it seems to be due to a non-linear
dose-response relation between exposure to tobacco smoke (either from
smoking or exposure to others people's smoke) and the risk of heart
disease. At low doses the risk increases rapidly, at high doses more
slowly. The authors estimate that, after adjustment for dietary
confounding, the excess risk of ischaemic heart disease from exposure
to environmental tobacco smoke is 23%. They consider that they have
made a persuasive case for ischaemic heart disease to be added to the
list of diseases caused by passive smoking. On page 980 Hackshaw et al
examine the effects of environmental tobacco smoke on risk of lung
cancer. The analysis, based on 39 epidemiological studies (three times
as many as the initial meta-analysis published in 1986), shows an
excess risk of lung cancer of 24% in non-smokers who live with
smokers, an effect that cannot be explained by bias or confounding. The
causal association is supported by a dose-response relation between
risk of lung cancer among non-smokers and years of living with a smoker
and the amount smoked by her or him; by the fact that the risk is
proportional to that in smokers given the difference in dose; and by
the finding of tobacco specific carcinogens in the blood and urine of
non-smokers exposed to other people's smoke. The authors conclude that
their analysis confirms that exposure to environmental tobacco smoke is
a cause of lung cancer.
Infertility is considered to be a risk factor for testicular germ
cell neoplasia. Giwercman et al (p 989) carried out a prospective
study on a consecutive group of 207 men referred because of
infertility. All the men had sperm counts under 10 x 106/ml
or below 20 x 10[6/ml and a history of cryptorchidism
or atrophic testicles and underwent bilateral testicular biopsy. None
of the 207 men had carcinoma in situ of the testis (a precursor of
invasive tumour). The authors conclude that infertile men with moderate
oligozoospermia may not be at high risk of testicular cancer, but this
risk may be significantly increased in men with very low sperm counts,
atrophic testes, and an irregular echo pattern on ultrasonography.
]
Bedside test for paracetamol poisoning gives inconsistent results
Rapid determination of paracetamol concentrations is obviously useful
in cases of suspected overdosage. Comparing the AcetaSite test with an
established laboratory method, Egleston et al (p 991) found
considerable discrepancies between the two methods - such that three out
of five patients whose results were outside the limits of agreement
would not have received treatment with the antidote, acetylcysteine.
The authors conclude that the bedside test should not replace the
standard assay.
Smoking has been associated with a lower risk of dying in hospital
after an acute myocardial infarction. In an analysis of over 5,000
coronary patients in New Zealand, Sonke et al confirmed this (p
992), but they found no overall effect of smoking on total case
fatality because of the larger effect of smokers who die before
admission to hospital than those who survive to be admitted.
Ex-smokers, however, had lower risks of dying both before and after
hospital admission.
Treating the obesity epidemic
Over half the British population is overweight; the health
benefits of even modest weight loss make a strong case for managing
obesity in its own right. On page 997 Wilding reviews the mechanisms
that control body weight and how these may lead to the development of
new treatments for obese people. A combination of genetics and
physiological studies is improving our understanding of the complex
mechanisms that control appetite and energy expenditure, but even
though drug and surgical treatments are likely to be used increasingly,
public health measures to alter lifestyles are vital.
Home | Current issue | Past issues |
Classified ads | Career Focus | Feedback
Collections |
About this site | About the BMJ | BMA | Medline
|
