In the last two centuries, age at menarche has decreased in several European populations, whereas adult height has increased. It is unclear whether these trends have ceased in recent years or how age at menarche and height are related in individuals. In this study, the authors first investigated trends in age at menarche and adult height among 286,205 women from nine European countries by computing the mean age at menarche and height in 5-year birth cohorts, adjusted for differences in socioeconomic status. Second, the relation between age at menarche and height was estimated by linear regression models, adjusted for age at enrollment between 1992 and 1998 and socioeconomic status. Mean age at menarche decreased by 44 days per 5-year birth cohort (beta = -0.12, standard error = 0.002), varying from 18 days in the United Kingdom to 58 days in Spain and Germany. Women grew 0.29 cm taller per 5-year birth cohort (standard error = 0.007), varying from 0.42 cm in Italy to 0.98 cm in Denmark. Furthermore, women grew approximately 0.31 cm taller when menarche occurred 1 year later (range by country: 0.13-0.50 cm). Based on time trends, more recent birth cohorts have their menarche earlier and grow taller. However, women with earlier menarche reach a shorter adult height compared with women who have menarche at a later age.

Objectives-To identify child or family related risk factors for unintentional childhood poisoning in Greece and to explore whether product specific poisonings might have special features that make them amenable to preventive interventions. Setting-A case-control study was undertaken in Athens, Greece in 1995. Cases were 100 consecutive children brought with poisoning to the emergency clinics of the two university affiliated children's hospitals. For every case two age, gender, and hospital matched controls were chosen from among children brought to the outpatient clinics of these hospitals on the same date. Methods-All children and their guardians were interviewed by the same person using a standard questionnaire that covered demographic, socioeconomic, behavioral, and past injury characteristics. Information was also obtained concerning type and conditions of poisoning for cases. Statistical analysis was undertaken by modeling the data using conditional logistic regression. Results-Socioeconomic factors were not important risk indicators in these data but children living with other than both parents were at increased risk (odds ratio (OR) = 4 7, p = 0 08), as were children with a history of previous poisoning that required medical care (OR = 5-1, p = 0-05). Unintentional poisonings caused by chewing or swallowing cigarettes were concentrated in families where both parents were smokers.Conclusions-Absence of a parent appears to be associated with increased likelihood of childhood poisoning. The importance of product accessibility is underlined by the concentration of tobacco poisoning among children of parents who were both smokers. In the cultural context of this study, sociodemographic factors do not appear to represent demonstrable risk factors.Instead, control of childhood poisoning should be concentrated on safe packaging, storage, and disposal of potentially hazardous products.(Injury Prevention 1996; 2: [208][209][210][211]

In the context of a large -scale molecular epidemiology study of biomarkers of genotoxicity of air pollution, 24 -h mean personal exposures to airborne PM 2.5 ( particulate matter < 2.5 m ) and associated polycyclic aromatic hydrocarbon ( PAHs ) were measured in 194 non -smoking technical institute students living in the city of Athens, Greece ( an area with moderately high levels of air pollution ) and the nearby small town of Halkida anticipated to have lower pollution levels. Extensive information relevant to the assessment of long -term and recent exposure to PAH was obtained from questionnaires as well as a time ± location ± activity diary ( TLAD ) which was kept by all subjects during a 4 -day observation period. During the last 24 h of this period, subjects underwent personal exposure monitoring for PM 2.5 and PAH, while a sample of blood was donated at the end of this period. All subjects were monitored in this way twice; once during a winter season ( October ± February ) and once during the following summer season ( June ± September ) . Nine subjects with plasma cotinine levels above 20 ng / ml were considered as unreported smokers and excluded from the study. Winter PM 2.5 exposures were lower in Athens ( geometric mean 39.7 g / m 3 ) than Halkida ( geometric mean 56.2 g / m 3 ) (P < 0.001 ) , while there was no significant location difference during the summer ( Athens: geometric mean 32.3 g / m 3 , Halkida: geometric mean 32.9 g / m 3 ; P= 0.79 ) . On the other hand, PAH exposures ( sum of the eight carcinogenic PAHs ) were significantly higher in Athens than in Halkida during the winter ( Athens: geometric mean 8.26 ng / m 3 , Halkida: geometric mean 5.80 ng / m 3 ; P < 0.001 ) as well as during the summer ( Athens: geometric mean 4.44 ng / m 3 , Halkida: geometric mean 1.48 ng / m 3 ; P < 0.001 ) . There was a significant difference in the profile of the PAH exposures at the two locations, the proportion of lighter PAH ( benzo This difference appeared to be related to individual exposure to environmental tobacco smoke ( ETS ) , as indicated by ( a ) the correlation at the individual level between the CHRYS / BPer ratio and declared time of recent exposure to ETS as well as plasma cotinine levels, especially during the winter; ( b ) the parallel variation of the mean levels of all three markers ( declared ETS exposure, cotinine levels, CHRYS / BPer ratio ) among three subgroups of subjects ( Athens subjects who had lowest levels of all three markers; Halkida subjects other than those living in the institute campus area; and Halkida subjects living in the institute campus area who had the highest levels of all three markers ) . This demonstrates that ETS can have a distinctive effect on the PAH exposure profile of subjects exposed to relatively low levels of urban air pollution.

CYP1A1 plays an important role in the metabolic activation of polycyclic aromatic hydrocarbons (PAH), carcinogenic components of air pollution. The influence of CYP1A1 genotype (*2A, *2B and *4) on the levels of lymphocyte bulky DNA adducts and the frequency of cells with aberrant chromosomes was assessed in 194 non-smoking subjects in whom recent exposure to environmental tobacco smoke (ETS) and airborne particulate-associated PAH were measured during two consecutive seasons (winter and summer). While CYP1A1*4 had no consistent effect on either biomarker of genetic damage, the levels of both biomarkers responded in a parallel fashion to changes in exposure/CYP1A1*2A genotype combinations during both seasons. Specifically, the levels of both biomarkers were increased in carriers of at least one CYP1A1*2A allele, as compared with CYP1A1*1 homozygotes, in subjects with ETS exposures >0.8 h/day during the previous 4 days and mean personal exposure to benzo[a]pyrene <0.9 ng/m3 during the previous 24 h (all P < 0.05). Outside these exposure limits the differential effect in CYP1A1*2A variants was lost. Although the numbers of subjects with the CYP1A1*2B polymorphism was small, the same trend appeared to be followed in this case. These effects are interpreted as resulting from differential induction of CYP1A1 expression in CYP1A1*2A and CYP1A1*2A/*2B carriers by components of ETS-polluted air at levels of exposure readily suffered by large segments of the general population and suggest that subjects with these genotypes may have increased susceptibility to the genotoxic effects of ETS.

We have investigated the relationship between consumption of food groups and intake of energy-generating macronutrients on the one hand, and birthweight on the other among apparently healthy singleton, term babies. Three hundred and sixty-eight women who delivered in six maternity clinics in two Greek cities during specified days over an 8-month period completed a 190-item, interviewer-administered, validated, semiquantitative food frequency questionnaire. Study participants also provided information on sociodemographic, reproductive and lifestyle variables. Data were analysed using multiple regression modelling. Nutritional variables were energy-adjusted, and non-nutritional correlates of birthweight were accounted for. The analysis revealed most of the established non-nutritional associations of birthweight -- an indication of study validity. Among food groups, meat and meat products and fish and sea food were suggestively associated with increased birthweight (two tailed P-values 0.08 and 0.16, respectively). Among energy-generating nutrients, monounsaturated fat was positively associated with birthweight and significantly so in several of the models. We consider our findings are considered as compatible with hypotheses linking fish and meat intake to fetal growth and as indicative of a positive association between intake of monounsaturated fat and birthweight.