Microhardness of composite materials with different organic phases in deep class II cavities: an in vitro study.

OBJECTIVE: This study compared the microhardness of three composite resins with different organic matrices in deep class II cavities. MATERIALS AND METHOD: A total of 36 extracted molars were randomly assigned to six groups and standardized class II cavities were prepared. The cavity design comprised three steps in a mesiodistal direction with an increasing depth (2, 4, and 6 mm). Twelve cavities each were restored using Filtek Supreme (FS), Quixfil (QF), and Filtek Silorane (SI). The materials were applied in incremental layers of 2 mm and cured either with Halogen Translux Energy (HTE) (n=18) or LED Bluephase C8 (LED) (n=18). Subsequently, the specimens were cross-sectioned, and microhardness was determined in various depths and at two different distances from the matrix. RESULTS: QF yielded the highest KHN microhardness values (92.67 ± 12.77), followed by FS (65.53 ± 19.52) and SI (57.67 ± 8.33). Composites cured with LED achieved higher KHN values. All materials showed the highest microhardness values within the superficial increments and at a distance of 1000 µm from the matrix.

Uncovering the effects of smoking: historical perspective.

Tobacco was introduced into Europe from America at the end of the fifteen century. At first used primarily for medicinal purposes it came to be burnt in pipes for pleasure on a large scale nearly 100 years later, at first in England and subsequently in Europe and throughout the world. Pipe smoking gave way to the use of tobacco as snuff and, in turn, to cigars and cigarettes at different times in different countries until cigarette smoking became the dominant form in most of the developed world between the two world wars. Societies were formed to discourage smoking at the beginning of the century in several countries, but they had little success except in Germany where they were officially supported by the government after the Nazis seized power. In retrospect it can now be seen that medical evidence of the harm done by smoking has been accumulating for 200 years, at first in relation to cancers of the lip and mouth, and then in relation to vascular disease and cancer of the lung. The evidence was generally ignored until five case-control studies relating smoking to the development of lung cancer were published in 1950. These stimulated much research, including the conduct of cohort studies, which, by the late 1950s, were beginning to show that smoking was associated with the development of many other diseases as well. The interpretation that smoking caused these various diseases was vigorously debated for some years but came to be generally accepted in respect of lung cancer by the late 1950s and of many other diseases in the subsequent two decades. Cigarette smoking has now been found to be positively associated with nearly 40 diseases or causes of death and to be negatively associated with eight or nine more. In some instances the positive associations are largely or wholly due to confounding, but the great majority have been shown to be causal in character. The few diseases negatively associated with smoking are for the most part rare or nonfatal and their impact on disease incidence and mortality as a result of smoking is less than 1% of the excess of other diseases that are caused by smoking. The most recent observations show that continued cigarette smoking throughout adult life doubles age-specific mortality rates, nearly trebling them in late middle age. All the diseases related to smoking that cause large numbers of deaths should now have been discovered, but further nonfatal diseases may remain to be revealed by cohort studies that are able to link individuals' morbidity data with their personal characteristics.

Estimation of dietary intake of nitrate and nitrite in Great Britain.

A survey was conducted of the dietary intake of nitrate and nitrite of 747 people aged 15-74 yr living in four regions in Britain. The mean intakes from food were estimated to be about 95 mg nitrate and 1.4 mg nitrite. Vegetables contributed over 90% of the nitrate intake and cured meats 65% of the nitrite intake. The contribution from drinking-water was estimated to add a further 13.5 mg, about 12% of total intake, but varied greatly depending upon water nitrate concentration. Residents of Oxford and the South-east had a higher intake of dietary nitrate, due to a greater vegetable consumption, whereas those from North Wales and the North-east had a higher nitrite intake due mainly to a greater consumption of bacon. The consumption of relatively low ascorbic acid/high nitrate vegetables was significantly greater in Oxford and the South-east. Smoking appeared to inhibit the uptake of circulating nitrate into the saliva, especially at higher levels of dietary nitrate intake. The efficiency of reduction of nitrate to nitrite in vivo and the effect of differing rates of this conversion on the relative importance of different dietary items as potential sources of nitrite are discussed.

Effects of exposure to vinyl chloride. An assessment of the evidence.

This paper reviews the possible effects of vinyl chloride on the mortality of occupationally exposed men and the carcinogenic effects that might be observed in the general population as a result of environmental pollution with vinyl chloride. The results of four studies fulfilling the criteria of providing substantial numbers of observations more than 25 years after first exposure and covering a period long enough for more than 10% of the workers to have been expected to die constitute the basis for the assessment of the occupational hazards. Other studies provide only supplementary information. The data permit two conclusions. First, men occupationally exposed to vinyl chloride have experienced a specific hazard of angiosarcoma of the liver. Second, any other occupational hazards that may have existed have been small. No positive evidence of a hazard of any nonmalignant disease or any type of cancer other than angiosarcoma of the liver has been found except possibly for a small hazard of lung cancer when exposure was heavy. More definite conclusions might be reached if those who have studied exposed employees could present their results in appropriate and comparable ways. A very small risk of angiosarcoma may have occurred as a result of vinyl chloride escaping into the environment around plants handling vinyl chloride in the past, but the evidence indicates that the current risk to the general public (if any) must be negligible.

Mortality in relation to smoking: 40 years' observations on male British doctors.

OBJECTIVE: To assess the hazards associated with long term use of tobacco. DESIGN: Prospective study of mortality in relation to smoking habits assessed in 1951 and again from time to time thereafter, with causes sought of deaths over 40 years (to 1991). Continuation of a study that was last reported after 20 years' follow up (1951-71). SUBJECTS: 34,439 British male doctors who replied to a postal questionnaire in 1951, of whom 10,000 had died during the first 20 years and another 10,000 have died during the second 20 years. RESULTS: Excess mortality associated with smoking was about twice as extreme during the second half of the study as it had been during the first half. The death rate ratios during 1971-91 (comparing continuing cigarette smokers with life-long non-smokers) were approximately threefold at ages 45-64 and twofold at ages 65-84. The excess mortality was chiefly from diseases that can be caused by smoking. Positive associations with smoking were confirmed for death from cancers of the mouth, oesophagus, pharynx, larynx, lung, pancreas, and bladder; from chronic obstructive pulmonary disease and other respiratory diseases; from vascular diseases; from peptic ulcer; and (perhaps because of confounding by personality and alcohol use) from cirrhosis, suicide, and poisoning. A negative association was confirmed with death from Parkinson's disease. Those who stopped smoking before middle age subsequently avoided almost all of the excess risk that they would otherwise have suffered, but even those who stopped smoking in middle age were subsequently at substantially less risk than those who continued to smoke. CONCLUSION: Results from the first 20 years of this study, and of other studies at that time, substantially underestimated the hazards of long term use of tobacco. It now seems that about half of all regular cigarette smokers will eventually be killed by their habit.

Mortality in relation to consumption of alcohol: 13 years' observations on male British doctors.

OBJECTIVE: To assess the risk of death associated with various patterns of alcohol consumption. DESIGN: Prospective study of mortality in relation to alcohol drinking habits in 1978, with causes of death sought over the next 13 years (to 1991). SUBJECTS: 12,321 British male doctors born between 1900 and 1930 (mean 1916) who replied to a postal questionnaire in 1978. Those written to in 1978 were the survivors of a long running prospective study of the effects of smoking that had begun in 1951 and was still continuing. RESULTS: Men were divided on the basis of their response to the 1978 questionnaire into two groups according to whether or not they had ever had any type of vascular disease, diabetes, or "life threatening disease" and into seven groups according to the amount of alcohol they drank. By 1991 almost a third had died. All statistical analyses of mortality were standardised for age, calendar year, and smoking habit. There was a U shaped relation between all cause mortality and the average amount of alcohol reportedly drunk; those who reported drinking 8-14 units of alcohol a week (corresponding to an average of one to two units a day) had the lowest risks. The causes of death were grouped into three main categories: "alcohol augmented" causes (6% of all deaths: cirrhosis, liver cancer, upper aerodigestive (mouth, oesophagus, larynx, and pharynx) cancer, alcoholism, poisoning, or injury), ischaemic heart disease (33% of all deaths), and other causes. The few deaths from alcohol augmented causes showed, at least among regular drinkers, a progressive trend, with the risk increasing with dose. In contrast, the many deaths from ischaemic heart disease showed no significant trend among regular drinkers, but there were significantly lower rates in regular drinkers than in non-drinkers. The aggregate of all other causes showed a U shaped dose-response relation similar to that for all cause mortality. Similar differences persisted irrespective of a history of previous disease, age (under 75 or 75 and older), and period of follow up (first five and last eight years). Some, but apparently not much, of the excess mortality in non-drinkers could be attributed to the inclusion among them of a small proportion of former drinkers. CONCLUSION: The consumption of alcohol appeared to reduce the risk of ischaemic heart disease, largely irrespective of amount. Among regular drinkers mortality from all causes combined increased progressively with amount drunk above 21 units a week. Among British men in middle or older age the consumption of an average of one or two units of alcohol a day is associated with significantly lower all cause mortality than is the consumption of no alcohol, or the consumption of substantial amounts. Above about three units (two American units) of alcohol a day, progressively greater levels of consumption are associated with progressively higher all cause mortality.

Further follow up of mortality and incidence of cancer in men from the United Kingdom who participated in the United Kingdom's atmospheric nuclear weapon tests and experimental programmes.

OBJECTIVES: To study the long term effects of participation in the United Kingdom's atmospheric nuclear weapon tests and experimental programmes and to test hypotheses generated by an earlier report, including the possibility that participation in tests caused small hazards of leukaemia and multiple myeloma. DESIGN: Follow up study of mortality and cancer incidence. SUBJECTS: 21,358 servicemen and civilians from the United Kingdom who participated in the tests and a control group of 22,333 non-participants. MAIN OUTCOME MEASURES: Numbers of deaths; standardised mortality ratios; relative risks of mortality from all causes and 27 types of cancer. RESULTS: During seven further years of follow up the numbers of deaths observed in participants were fewer than expected from national rates for all causes, all neoplasms, leukaemia, and multiple myeloma (standardised mortality ratios 0.86, 0.85, 0.57, and 0.46); death rates were lower than in controls (relative risks 0.99, 0.96, 0.57, and 0.57; 90% confidence intervals all included 1.00). In the period more than 10 years after the initial participation in tests the relative risk of death in participants compared with controls was near unity for all causes (relative risk 0.99 (0.95 to 1.04) and all neoplasms (0.95 (0.87 to 1.04)); it was raised for bladder cancer (2.69 (1.42 to 5.20)) and reduced for cancers of the mouth, tongue, and pharynx (0.45 (0.22 to 0.93)) and for lung cancer (0.85 (0.73 to 0.99)). For leukaemia mortality was equal to that expected from national rates but greater than in controls for both the whole follow up period (1.75 (1.01 to 3.06)) and the period 2-25 years after the tests (3.38 (1.45 to 8.25)). CONCLUSION: Participation in nuclear weapon tests had no detectable effect on expectation of life or on subsequent risk of developing cancer or other fatal diseases. The excess of leukaemia in participants compared with controls seems to be principally due to a chance deficit in the controls, but the possibility that participation in the tests may have caused a small risk of leukaemia in the early years afterwards cannot be ruled out.

Urban and rural factors in the aetiology of cancer.

The incidence of cancer, or the mortality attributed to it, has been compared in urban and rural residents in 13 populations. In each case, the incidence (or mortality) has been higher in the urban areas in each sex, the ratios varying from a minimum of 1.03 to 1 in men in Japan to 1.63 to 1 in men in Denmark. Examination of 26 separate types of cancer showed that 23 tended to be more common in towns, 1 (myeloma) to be evenly distributed, and 2 (cancers of the lip and eye) to be more common in the countryside. The urban excess was greatest for cancers of the bladder, larynx, liver, lung, mouth and pharynx, and oesophagus, and least for leukaemia and non-Hodgkin's lymphoma. It is concluded that differences in personal behaviour (cigarette smoking, alcohol consumption, sexual promiscuity, exposure to ultraviolet light, type of diet, and family size) are the principal factors responsible for the urban excess. Other factors include general atmospheric pollution, occupational hazards, genetic differences in susceptibility, and artefacts of diagnosis and recording. The rural excess was marked for cancer of the lip in both sexes, but less marked and clearly evident only in men for cancer of the eye. Three-quarters of eye cancers are melanomas and the excess incidence in rural areas provides some weak support for the idea that exposure to sunlight contributes to the production of the disease.

Pott and the path to prevention.

Two hundred years ago, Percival Pott, a London surgeon, recognized that chimney sweeps were particulary liable to develop scrotal cancer and attributed the disease to exposure to soot. By so doing, he described the first environmental cause of cancer and started the chain of events that led to the first experimental production of cancer, the first synthesis of a carcinogen, and the first isolation of a carcinogen from a natural substance. Following these laboratory successes, the main object of cancer research has been to discover the fundamental characteristics of the cancer cell and the mechanism of the cancer cell and the mechanism of its production and relativly few investigations have studied the conditions under which cancer is produced in man. Recently, however, it has been recognized that we can often prevent cancer by modifying the conditions of life without detailed knowledge of the mechanism of carcinogenesis. All but a few rare cancers vary in incidence with place or time or with both and nearly all this variation can be shown to be environmental in origin. We already know enough to prevent most cancers of the mouth, oesophagus, larynx, lung, bladder, and skin in W. Europe and N. America, most cancers of the mouth in Asia, and most liver cancers in Africa. We have clues to the causation of cancer of the cervix uteri, breast, and colon and we should learn how to prevent all these cancers before long. Many new hazards could be prevented by controlling the introduction of new carcinogenic chemicals into the environment while others could be detected quickly by improved methods of epidemiological enquiry. But even so, acute clinical observers, like Pott, will continue to be needed for many years.

Fluoridation of water and cancer mortality in the U.S.A.

Authoritative statements that fluoridation of public water supplies is not associated with any increase in cancer have been challenged on the basis of data which, it is claimed, show that cancer mortality in the United States rose more sharply in cities with fluoridated water than in those without. However, during the period of study (1950-70) the population structures of these cities changed substantially. When account is taken of age, sex, and ethnic group the ratio between observed cancer mortality and expected cancer mortality fell slightly in the cities with fluoridated water and did not change in the non-fluoridated cities.

Cancers of the respiratory tract in mustard gas workers.

In a study of a cohort of 2498 men and 1032 women employed in the manufacture of mustard gas in Cheshire during the second world war 3354 (95%) individuals were successfully traced for mortality to the end of 1984. Large and highly significant excesses were observed as compared with national death rates for deaths from cancer of the larynx (11 deaths observed, 4.04 expected, p = 0.003), pharynx (15 observed, 2.73 expected, p less than 0.001), and all other buccal cavity and upper respiratory sites combined (lip, tongue, salivary gland, mouth, nose) (12 observed, 4.29 expected, p = 0.002). For lung cancer, a highly significant but more moderate excess was observed (200 observed, 138.39 expected, p less than 0.001). Significant excesses were also observed for deaths from acute and chronic non-malignant respiratory disease (131 observed, 91.87 expected and 185 observed, 116.31 expected, respectively). The risks for cancers of the pharynx and lung were significantly related to duration of employment. None of these results is substantially altered when expected numbers are calculated from Cheshire urban areas rather than national rates, although the relative risks for lung cancer and non-malignant respiratory disease are substantially reduced if rates for Merseyside, the nearest large conurbation, are used. The results provide strong evidence that exposure to mustard gas can cause cancers of the upper respiratory tract and some evidence that it can cause lung cancer and non-malignant respiratory disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Geographic and social class variation within the UK in levels of salivary nitrates and nitrites. A preliminary report.

In the study, the first results of which are reported here, salivary nitrate and nitrite levels were examined in populations drawn from regions of the UK which differ in mortality rates for gastric cancer. The aims were to see, firstly, whether there was an equivalent geographic variation for nitrate and nitrite levels and, secondly, whether within each region any socio-economic or dietary characteristics correlated with the salivary levels. The results show that the nitrate and nitrite levels are significantly higher in residents from the Oxford region (low gastric cancer incidence area) than in residents from the north-east of England and north Wales (high-incidence areas). Further, within each area there is a noticeable relationship between nitrate and nitrite levels and age and social class. The social class trend is, as with the geographic trend, the inverse of that for stomach cancer risk. It is felt that the explanation of these results is probably a greater consumption of fresh, nitrate-containing vegetables by people in the Oxford region and by those in higher socio-economic groups. The implications that these results have for the nitrate hypothesis in relation to gastric cancer is discussed.

Nitrates, nitrites and gastric cancer in Great Britain.

Nitrate and nitrite were measured in the saliva of two populations who differed in their risk of developing gastric cancer. Surprisingly, the levels of both ions were significantly higher in the low-risk group.

Exposure to vinyl chloride and angiosarcoma of the liver: a report of the register of cases.

The Association of Plastic Manufacturers in Europe maintains a register of all cases of angiosarcoma of the liver (ASL) resulting from exposure to vinyl chloride monomer (VCM). This register has recorded all known VCM related cases of the disease worldwide that have been histologically confirmed. Although likely to be incomplete, it is the most comprehensive tabulation of such cases available and, by the end of 1984, 118 men had been registered. The information from analysis of the cases currently on the register is used to make an approximate projection of the number of cases to be expected in the future. The conclusion from this projection is that the industry is reaching the halfway stage in the appearance of VCM related ASL.

Mortality of nitrate fertiliser workers.

An epidemiological cohort study was conducted to investigate the mortality patterns among a group of workers engaged in the production of nitrate based fertilisers. This study was designed to test the hypothesis that individuals exposed to high concentrations of nitrates might be at increased risk of developing cancers, particularly gastric cancer. A total of 1327 male workers who had been employed in the production of fertilisers between 1946 and 1981 and who had been occupationally exposed to nitrates for at least one year were followed up until 1 March 1981. In total, 304 deaths were observed in this group and these were compared with expected numbers calculated from mortality rates in the northern region of England, where the factory was located. Analysis was also carried out separately for a subgroup of the cohort who had been heavily exposed to nitrates--that is, working in an environment likely to contain more than 10 mg nitrate/m3 for a year or longer. In neither the entire cohort nor the subgroup was any significant excess observed for all causes of mortality or for mortality from any of five broad categories of cause or from four specific types of cancer. A small excess of lung cancer was noted more than 20 years after first exposure in men heavily exposed for more than 10 years. That men were exposed to high concentrations of nitrate was confirmed by comparing concentrations of nitrates in the saliva of a sample of currently employed men with control men, employed at the same factory but not in fertiliser production. The men exposed to nitrate had substantially raised concentrations of nitrate in their saliva compared with both controls within the industry and with men in the general population and resident nearby. The results of this study therefore weight against the idea that exposure to nitrates in the environment leads to the formation in vivo of material amounts of carcinogens.