Mental health in girls and boys exposed to intimate partner violence.

OBJECTIVES: Children of abused women have a greater risk of mental health problems. This study assesses the association between women's exposure to intimate partner violence (IPV) and the mental health of their children in the population of the Madrid Region. STUDY DESIGN: Cross-sectional. METHODS: Data were drawn from the '2014 Survey on Intimate Partner Violence against Women in the Madrid Region'. Women meeting the definition of IPV answered the Strengths and Difficulties Questionnaire (SDQ) on the mental health of one of their children aged 4-16 years. The comparison group was made up of mother-child dyads that had not been exposed to IPV. We used multivariate analysis to assess whether the children of abused women had a greater probability of having higher SDQ subscale and total scores. RESULTS: A total of 209 mother-child dyads were analyzed, 64 exposed (50% boys) and 145 unexposed to IPV (51% boys). Exposure to IPV was associated with a high SDQ score (greater risk of mental health problems), with a prevalence ratio of 3.6 (95% CI 1.2-10.3) in girls and 2.4 (95% CI 1.1-5.1) in boys. Among girls, moreover, exposure to IPV was significantly associated with behavioral and inattention/hyperactivity problems. In conclusion, exposure to IPV was associated with an increased frequency of mental health problems among children in general, and girls in particular. CONCLUSIONS: This study reinforces the recommendations to conduct studies with data disaggregated by sex and to address the impact of IPV in mothers and children jointly.

Increase in socioeconomic inequalities in mortality in a Southern European region: a small-area ecological study.

BACKGROUND: This study sought to describe the total mortality trend by socioeconomic deprivation (SED) in the Madrid Autonomous Region, by sex and age group. METHODS: Cross-sectional ecological study by census tract, in two periods: 1994-2000 (P1) with SED of 1996 census and 2001-07 (P2) with SED of 2001 census. We calculated the relative risks (RRs) and their 95% credibility intervals (95% CIs) by SED quintile (Q), taking the quintile of least deprivation as reference. Besag-York-Mollié ecological regression models and the Integrated Nested Laplace Approximation procedure were applied. The absolute differences in age-standardized rates were compared by SED quintile. RESULTS: Inequalities decreased in young adults: among men aged 20-39 years, the RR in Q5 versus Q1 ranged from 2.73 (95% CI, 2.51-3.02) in P1 to 1.93 (95% CI, 1.76-2.15) in P2, due to the greater improvement in the most underprivileged groups. In contrast, there was an increase in SED-related mortality in the 40-79 age group. Among men aged 40-59 years, the RR in Q5 versus Q1 rose from 1.88 (95% CI, 1.76-2.02) in P1 to 2.29 (95% CI, 2.17-2.43) in P2; the improvement was greater in the most privileged groups. CONCLUSION: In a context of an economic boom, inequalities were observed to increase among adults by a greater improvement in the most privileged groups.

Evolution of socio-economic inequalities in mortality in small geographical areas of the two largest cities in Spain (Barcelona and Madrid), 1996-2007.

OBJECTIVES: To describe the evolution of socio-economic inequalities in mortality in small areas of two Spanish cities (Barcelona and Madrid) from 1996 to 2001 and from 2002 to 2007. STUDY DESIGN: A small-area ecological study of trends was performed, in which the units of analysis were census tracts. METHODS: The association between mortality and socio-economic deprivation was assessed through Poisson regression analysis. Models were stratified by sex, age group and period of study. The trend in inequalities in mortality was assessed by introducing an interaction term between deprivation and the period of study. RESULTS: Mortality in the most-deprived areas was significantly higher than mortality in the less-deprived areas in both periods and most age groups. However, inequalities seemed to diminish in young people and elderly women, especially in Barcelona. CONCLUSIONS: There is a need to monitor inequalities in mortality in the near future because the current financial crisis could change this situation.

Regulation of cell surface beta 1 integrin levels during keratinocyte terminal differentiation.

Integrins of the beta 1 family play a central role in controlling adhesion and terminal differentiation within the epidermis. When human epidermal keratinocytes undergo terminal differentiation, intracellular transport of newly synthesized integrins is inhibited, and mature receptors are lost from the cell surface. We have examined the mechanisms underlying these processes, using an experimental model in which keratinocytes are placed in suspension to induce terminal differentiation. The block in intracellular transport was keratinocyte- and integrin-specific since it was not observed when fibroblasts were placed in suspension and did not affect E-cadherin synthesis in suspended keratinocytes. Newly synthesized beta 1 integrins associated with an endoplasmic reticulum resident protein, calnexin; the association was prolonged when keratinocytes were placed in suspension, suggesting a role for calnexin in the inhibition of transport. After 24 h, the level of beta 1 integrin mRNA declines in suspended keratinocytes, reflecting inhibition of gene transcription, but in fibroblasts, the level remained constant. Transport of integrins could be blocked in both adherent keratinocytes and fibroblasts by inhibiting total protein synthesis, raising the possibility that transport is coupled to de novo integrin synthesis. The fate of receptors on the surface of keratinocytes was followed by confocal immunofluorescence microscopy, immunoelectron microscopy, and biochemical analysis: with the onset of terminal differentiation, endocytosed receptors were transported to the lysosomes. These experiments reveal novel mechanisms by which integrin levels can be controlled. Together with our earlier evidence for transcriptional regulation and affinity modulation of integrins, they highlight the complexity of the mechanisms which ensure that the onset of terminal differentiation is linked to detachment of keratinocytes from the underlying basement membrane.

FOXM1 allows human keratinocytes to bypass the oncogene-induced differentiation checkpoint in response to gain of MYC or loss of p53.

Tumour suppressor p53 or proto-oncogene MYC is frequently altered in squamous carcinomas, but this is insufficient to drive carcinogenesis. We have shown that overactivation of MYC or loss of p53 via DNA damage triggers an anti-oncogenic differentiation-mitosis checkpoint in human epidermal keratinocytes, resulting in impaired cell division and squamous differentiation. Forkhead box M1 (FOXM1) is a transcription factor recently proposed to govern the expression of a set of mitotic genes. Deregulation of FOXM1 occurs in a wide variety of epithelial malignancies. We have ectopically expressed FOXM1 in keratinocytes of the skin after overexpression of MYC or inactivation of endogenous p53. Ectopic FOXM1 rescues the proliferative capacity of MYC- or p53-mutant cells in spite of higher genetic damage and a larger cell size typical of differentiation. As a consequence, differentiation induced by loss of p53 or MYC is converted into increased proliferation and keratinocytes displaying genomic instability are maintained within the proliferative compartment. The results demonstrate that keratinocyte oncogene-induced differentiation is caused by mitosis control and provide new insight into the mechanisms driving malignant progression in squamous cancer.

Diabetes mellitus mortality in Spanish cities: Trends and geographical inequalities.

AIM: To analyze the geographical pattern of diabetes mellitus (DM) mortality and its association with socioeconomic factors in 26 Spanish cities. METHODS: We conducted an ecological study of DM mortality trends with two cross-sectional cuts (1996-2001; 2002-2007) using census tract (CT) as the unit of analysis. Smoothed standardized mortality rates (sSMR) were calculated using Bayesian models, and a socioeconomic deprivation score was calculated for each CT. RESULTS: In total, 27,757 deaths by DM were recorded, with higher mortality rates observed in men and in the period 1996-2001. For men, a significant association between CT deprivation score and DM mortality was observed in 6 cities in the first study period and in 7 cities in the second period. The highest relative risk was observed in Pamplona (RR, 5.13; 95% credible interval (95%CI), 1.32-15.16). For women, a significant association between CT deprivation score and DM mortality was observed in 13 cities in the first period and 8 in the second. The strongest association was observed in San Sebastián (RR, 3.44; 95%CI, 1.25-7.36). DM mortality remained stable in the majority of cities, although a marked decrease was observed in some cities, including Madrid (RR, 0.67 and 0.64 for men and women, respectively). CONCLUSIONS: Our findings demonstrate clear inequalities in DM mortality in Spain. These inequalities remained constant over time are were more marked in women. Detection of high-risk areas is crucial for the implementation of specific interventions.

The EGF receptor ligand amphiregulin controls cell division via FoxM1.

Epidermal growth factor receptor (EGFR) is central to epithelial cell physiology, and deregulated EGFR signaling has an important role in a variety of human carcinomas. Here we show that silencing of the EGF-related factor amphiregulin (AREG) markedly inhibits the expansion of human keratinocytes through mitotic failure and accumulation of cells with ⩾ 4n DNA content. RNA-sequencing-based transcriptome analysis revealed that tetracycline-mediated AREG silencing significantly altered the expression of 2331 genes, 623 of which were not normalized by treatment with EGF. Interestingly, genes irreversibly upregulated by suppression of AREG overlapped with genes involved in keratinocyte differentiation. Moreover, a significant proportion of the irreversibly downregulated genes featured upstream binding sites recognized by forkhead box protein M1 (FoxM1), a key transcription factor in the control of mitosis that is widely dysregulated in cancer. The downregulation of FoxM1 and its target genes preceded mitotic arrest. Constitutive expression of FoxM1 in AREG knockdown cells normalized cell proliferation, reduced the number of cells with ⩾ 4n DNA content and rescued expression of FoxM1 target genes. These results demonstrate that AREG controls G2/M progression and cytokinesis in keratinocytes via activation of a FoxM1-dependent transcriptional program, suggesting new avenues for treatment of epithelial cancer.

Changes in expression of members of the fos and jun families and myc network during terminal differentiation of human keratinocytes.

Normal human epidermal keratinocytes are induced to undergo terminal differentiation when disaggregated and placed in suspension: commitment occurs at about 5 h and overt differentiation by 24 h. In contrast, the squamous cell carcinoma line SCC12B2 does not initiate terminal differentiation until 75 h in suspension and the ndk strain of keratinocytes undergoes growth arrest but does not differentiate at all. In order to identify genes that may regulate terminal differentiation we have examined mRNA levels of members of the fos and jun gene families and myc gene network in suspension cultures of normal keratinocytes, SCC12B2 and ndk. The major changes observed were an up-regulation of c-Fos and Fra-1 and a decrease in c-Myc at the time of commitment, followed by an increase in Mad, Mxi1, Fra-2 and JunB expression at the onset of differentiation. The sequence of events shows a striking similarity to that which occurs during myeloid differentiation and suggests a role for AP-1 complexes and Myc and Mad complexes in regulating keratinocyte differentiation.

Normal and c-Myc-promoted human keratinocyte differentiation both occur via a novel cell cycle involving cellular growth and endoreplication.

The relationship between cell cycle and differentiation in human keratinocytes is poorly understood. It is believed that keratinocytes suppress DNA replication and cell cycle arrest in G0 before they initiate terminal differentiation. However, a temporal separation between both events has not been established. Moreover, c-Myc promotes keratinocyte differentiation without causing cell cycle arrest. To address these paradoxes we have analysed cell cycle control during normal and c-Myc-promoted differentiation. Continuous activation of c-Myc or initiation of terminal differentiation results in a block of G2/M, cellular growth, endoreplication and polyploidy. Keratinocytes abandon G1, continue replicating DNA as they differentiate terminally and become polyploid. In fact, simply blocking mitosis with nocodazole resulted in increased cell size, terminal differentiation and endoreplication. This indicates that terminal differentiation associates with defective cell cycle progression and provides a novel insight into c-Myc biology.

Switch from p53 to MDM2 as differentiating human keratinocytes lose their proliferative potential and increase in cellular size.

p53 transcription factor is mutated in most skin cell carcinomas and in more than 50% of all human malignancies. One of its transcriptional targets is MDM2, which in turn down-regulates p53. The role of the p53/MDM2 regulatory loop upon genotoxic stress is well documented, but less is known about its role in normal tissue homeostasis. We have explored this pathway during the different transitions of the human epidermal differentiation programme and after isolating stem cells, transit amplifying cells or differentiating cells from epidermis. Maximum expression of p53 was found in proliferating keratinocytes. A striking and transient induction of MDM2 and a down-modulation of p53 characterized the transition from proliferation to differentiation in primary human keratinocytes. These changes were delayed in late differentiating carcinoma cells, and were clearly different in suspended primary fibroblasts. Interestingly, these changes correlated with an increase in cell size, at the time of irreversible commitment to differentiation. Induction of MDM2 was also associated with suppression of proliferation in normal, or hyperproliferative, psoriatic epidermis. Moreover, both proteins were induced as keratinocytes were driven to leave the stem cell compartment by c-Myc activation. Overall, our results show a critical regulation of the p53/MDM2 pathway at the epidermal transition from proliferation to differentiation.

[Trends and social inequalities in cervical cancer and breast cancer screening in Madrid: Non-Commumicable Disease Risk FactorSurveillance System (SIVFRENT-A) from 1995 to 2010]. / Tendencias y desigualdades sociales en el cribado de cáncer de cérvix y cáncer de mama en la Comunidad de Madrid duranteel periodo 1995-2010 a partir del Sistema de Vigilancia deFactores de Riesgo de enfermedades no transmisibles (SIVFRENT-A).

BACKGROUND: The assessment of preventive programs is necessary to support the decisions made in public health. There are few research studies that evaluate the degree of implementation and equity of cancer screening in Spain. The objective was to describe trends and inequalities in cervical and breast cancer screening according social determinants of health. METHODS: An analysis was carried out on the Behavioral Risk Factor Surveillance System of Community of Madrid data, obtained between 1995 and 2000 from telephone surveys conducted on a population between ages 18 to 65, were analyzed. The years were grouped into four periods: P1 to P4. The trends were estimated with prevalence ratios (PR) with 95% confidence intervals (95% CI), obtained through generalized linear models with binomial family and logarithmic link. The inequalities were estimated with differences of proportions (DP) with 95% CI. RESULTS: An increased in mammograms is seen especially in women with low education (PR P4/P1: 1.93; 95%CI 1.62 to 2.3), this trend more discreet in cytology (PR P4/P1: 1.28; 95%CI 1.11 to 1.47). However mammograms have not increased over in the past 5 years (PR P4/P3: 1.02; 95% CI 0.99 to 1.04). Inequalities get better, but show an increase in the last period. CONCLUSIONS: All groups increase in preventative behaviors and those who did not, had a high prevalence from the start.Itis worth mentioning the stagnation of mammography in disadvantaged women in the period 2007-2010. There was a social gradient for preventive preventative measures, which was lower in the population-basedscreening (mammography) than in the opportunistic one (cytology).

Leukemia, lymphomas, and myeloma mortality in the vicinity of nuclear power plants and nuclear fuel facilities in Spain.

Mortality due to hematological tumors in towns near Spain's seven nuclear power plants and five nuclear fuel facilities during the period 1975-1993 was ascertained. The study was based on 610 leukemia-, 198 lymphoma-, and 122 myeloma-induced deaths in 489 towns situated within a 30-km radius of such installations. As control areas, we used 477 towns lying within a 50- to 100-km radius of each installation, matched by population size and a series of sociodemographic characteristics (income level, proportion of active population engaged in farming, proportion of unemployed, percentage of illiteracy, and province). Relative risk (RR) for each area and the trends in risk with increasing proximity to an installation were analyzed using log-linear models. None of the nuclear power plants registered an excess risk of leukemia-induced mortality in any of the surrounding areas. Excess risk of leukemia mortality was, however, observed in the vicinity of the uranium-processing facilities in Andújar [RR, 1.30; 95% confidence interval, 1.03-1.64] and Ciudad Rodrigo (RR, 1.68; 95% confidence interval, 0.92-3.08). Excess risk of multiplemyeloma mortality was found in the area surrounding the Zorita nuclear power plant. Statistical testing revealed that, with the single exception of multiple myeloma, none of the tumors studied showed evidence of a rise in risk with proximity to an installation. No study area yielded evidence of a raised risk of leukemia mortality among persons under the age of 25 years. More specific studies are called for in areas near installations that have been fully operational for longer periods. In this connection, stress should be laid on the importance of using dosimetric information in all future studies.

Epidermal differentiation, apoptosis, and senescence: common pathways?

Regulation and execution of epidermal terminal differentiation, apoptosis and cellular senescence share some molecular and cellular features. The three phenomena result in suppression of proliferation and in some instances they seem to overlap. The boundaries between keratinocyte terminal differentiation and senescence are unclear and the former has been proposed to be a form of apoptosis. However, cumulative evidence argues that they are alternative, independent responses to different stimuli. I summarize in this review classical and recent evidence underlying the molecular control of these biological processes and propose a rationale to understand their nature and function in epidermis.

Expression of intermediate filament proteins by normal and transformed mouse epidermal-keratinocytes in culture.

The aberrant expression of embryonic simple epithelial keratins K8 and K18 has been previously detected in chemically-induced mouse skin carcinomas and in cultured epidermal keratinocytes containing H-ras oncogenes. In this study, we report that cell lines derived from benign papillomas do not generally synthesize simple epithelial keratins, regardless of the presence of H-ras gene alterations. These results reinforce our previous suggestion that the expression of these keratins during mouse epidermal carcinogenesis is a marker of malignant transformation. The comparison of the two-dimensional electrophoresis intermediate filament protein profiles of transformed keratinocytes in culture, reveal that during in vitro progression to the malignant phenotype increased synthesis of simple epithelial keratins is associated to a general disturbance on the expression of cytoskeletal proteins.

[Validation of self-reported weight and height in an adolescent population]. / Validación del peso y la talla autodeclarados en población adolescente.

INTRODUCTION: The aim of this study was to examine the relationship between self-reported population in order to evaluate the validity of self-reported measures for the purpose of estimating the prevalence of low (less-than-or-equal 15th percentile) and high (greater-than-or-equal 85th percentile) body mass index (BMI) in the study population. SUBJECTS AND METHOD: Information on self-reported and objective weight and height was obtained from a representative sample of 3,244 adolescents, aged 15-18 years, in secondary education schools in the Autonomous Community of Madrid. We calculated the mean relative error; the correlation between subjective and objective parameters, sensitivity, specificity and predictive value positive of low and high BMIs. RESULTS: The mean relative errors were as follows: weight: +0.07% for males versus and 0.79% for females; height, +0.51% for males versus +0.98% for females; BMI: 0.88% for males versus 2.63% for females. The correlation between self-reported and objective BMI was 0.87 for males and 0.90 for females. The prevalence of high BMI was underestimated by 34.1% and 34.4% of females white that of low BMI was overestimated by 10.7% of males and 14.8% of females. CONCLUSION: Analysis of BMI as a continuous variable, based on self-reported weight and height measurement data, entails a small margin of error. However, its use as a categorical variable involves a considerable underestimate of the prevalence of high BMI, and an smaller overestimate of the prevalence of low BMI.

[Air pollutants and their monitoring]. / Contaminantes atmosféricos y su vigilancia.

Some basic concepts regarding air pollution are set out. Although, from a health care standpoint, our interest revolves around the impact which pollution has on human health, it being important to ascertain the main pollutants, the sources of emissions, the physiochemical properties thereof, the sampling and analysis methods which are used at the air pollution control stations, the limits set by the laws currently in impact and the World Health Organization recommendations with regard to the levels of immission. This study reviews these concepts with regard to the pollutants which have been analyzed in the Spanish Multicenter Study of Air Pollution and Mortality (EMECAM): particles, sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO) and ozone (O3). For this purpose, the most recent publications on this subject have been used, including part of what is going to be the line around which all of the measures aimed at combating air pollution are going to be revolving in the very near future, that is, the new set of European Union Directives (some currently in the proposal stage) and the latest recommendations (not as yet published) of the World Health Organization. Lastly, a wide range of aspects are set out which involve Public Health in the field of air pollution, despite the monitoring and control thereof falling to the environmental affairs authorities in terms of government organization.

Cyclin E drives human keratinocyte growth into differentiation.

Human epidermis is continuously exposed to environmental mutagenic hazard and is the most frequent target of human cancer. How the epidermis coordinates proliferation with differentiation to maintain homeostasis, even in hyperproliferative conditions, is unclear. For instance, overactivation of the proto-oncogene MYC in keratinocytes stimulates differentiation. Here we explore the cell cycle regulation as proliferating human keratinocytes commit to terminal differentiation upon loss of anchorage or overactivation of MYC. The S-phase of the cell cycle is deregulated as mitotic regulators are inhibited in the onset of differentiation. Experimental inhibition of mitotic kinase cdk1 or kinases of the mitosis spindle checkpoint Aurora B or Polo-like Kinase, triggered keratinocyte terminal differentiation. Furthermore, hyperactivation of the cell cycle by overexpressing the DNA replication regulator Cyclin E induced mitosis failure and differentiation. Inhibition of Cyclin E by shRNAs attenuated the induction of differentiation by MYC. In addition, we present evidence that Cyclin E induces DNA damage and the p53 pathway. The results provide novel clues for the mechanisms committing proliferative keratinocytes to differentiate, with implications for tissue homeostasis maintenance, HPV amplification and tumorigenesis.

Deaths in collective dwellings and inequalities in small-area mortality: an ecological study in the Madrid region (Spain).

BACKGROUND: Increasing numbers of elderly persons reside and die in institutions, yet there are few studies that analyse the effect of this on mortality in small areas and its ensuing effect on the association between material deprivation and mortality. METHODS: A cross-sectional, ecological study in the region of Madrid covering 3906 census tracts (median 1000 inhabitants), using mortality data for 1996-2003 and socioeconomic deprivation from the 2001 census. Standardised mortality ratios (SMR) were calculated for each census tract. Using the Besag-York-Mollié model, RR of dying and their 95% CI according to the deprivation index considered (with the fourth quartile, Q, being the most unfavourable situation) were calculated for deaths among: the total population and the population excluding residents who died in institutions. RESULTS: 6% of the deceased had been residing in institutions, which affected 16.5% of census sections (644) and accounted for 17% of the variability in SMR among men and 10% among women, p<0.001. Mortality increased with socioeconomic deprivation, whereas the RR for the total population in Q4 with respect to Q1 was 1.46 among men (95% CI 1.41 to 1.50) and 1.12 among women (95% CI 1.08 to 1.17), these figures rose to 1.48 (95% CI 1.43 to 1.53) and 1.14 (95% CI 1.10 to 1.18), respectively, for the population excluding residents who died in institutions. CONCLUSIONS: Deaths of residents in institutions affect the variation in small-area mortality, and confound the relationship between mortality and socioeconomic deprivation. This variable should be recorded in mortality statistics so that its effect can be controlled for in subsequent analyses.

Census tract socioeconomic and physical environment and cardiovascular mortality in the Region of Madrid (Spain).

BACKGROUND: Features of the area might contribute to differences in cardiovascular mortality. The census tract distribution of ischaemic heart disease (IHD) and cerebrovascular disease mortality in the Region of Madrid and its association with deprivation and environmental variables were examined in this study. METHODS: Cross-sectional, ecological study covering 3906 census tracts (median of around 1000 inhabitants), using mortality data (population aged <75 years) for 1996-2003, as well as socioeconomic deprivation and other environmental indicators (subjective perceptions of pollution, background noise, lack of green spaces and delinquency) drawn from the 2001 census. Standardised mortality ratios were calculated. Smoothed census tract relative risks were calculated using the Besag-York-Mollié model. Relative risks (RRs) of dying and their 95% credibility intervals (95% CI) were calculated according to the indicators considered (with the fourth quartile, Q, being the most unfavourable situation). Maps were plotted depicting the distribution of the posterior probability of RR>1. RESULTS: Census tracts with excess mortality were mostly located in the city of Madrid. Mortality increased with deprivation: RRs of IHD and stroke mortality in Q4 with respect to Q1 were 1.42 (95% CI 1.31 to 1.54) and 1.66 (95% CI 1.45 to 1.88) for men, and 1.54 (95% CI 1.33 to 1.79) and 1.52 (95% CI 1.29 to 1.76) for women respectively. Associations with deprivation decreased only slightly when perceived lack of green spaces and delinquency were included in the model. In men, subjective perceptions of areas remained associated with cardiovascular mortality after adjustment for deprivation. CONCLUSION: Deprivation and subjective perceptions of physical environmental characteristics are ecologically associated with cardiovascular disease mortality.

Chronic liver disease and cirrhosis mortality and social deprivation: a spatial analysis in small areas of Madrid region.

OBJECTIVES: To study census-tract distribution of chronic liver disease and cirrhosis mortality in the Madrid Region and its association with socio-economic deprivation. METHODS: Cross-sectional, ecological (3906 census-tract) study, using mortality data for 1996-2003 and a deprivation index drawn up on the basis of 2001 census data. Standardised mortality ratios were calculated taking Spanish rates for 2001 as reference. Smoothed census-tract relative risks were computed using the Besag-York-Mollie model. Relative risks (RRs) of dying and their 95% credibility intervals (95% CIs) were calculated according to quartiles of the deprivation index (with the fourth quartile -Q- of the indicator being the most unfavourable situation). Maps were plotted depicting the distribution of the posterior probability of RR > 1. RESULTS: Census tracts with a high risk of mortality were detected, mostly located in the centre and on the eastern, south-eastern and south-western fringes of the city of Madrid. Mortality increased with deprivation. RRs of mortality according to quartíles of the deprivation index were: Q2 = 1.5 (CI: 1.3-1.6), Q3 = 1.9 (CI:1.7-2.2) and Q4 = 2.5 (CI:2.2-2.8) for men; and Q2 = 1.3 (CI:1.1-1.5), Q3 = 1.5 (CI:1.3-1.7) and Q4 = 1.6 (CI:1.3-1.8) for women. CONCLUSIONS: This small-area study enabled census tracts with excess mortality eligible for a special public health intervention to be identified, and their association with socio-economic deprivation to be confirmed.