Lovasi et al. [1]) document the relationship between the density of
street trees and the prevalence of childhood asthma in New York City.
Their findings suggest street trees are associated with a lower
prevalence, although no causality was inferred. I would like to point out
a number of methodological issues which should benefit future studies on
this subject.
Prevalence of asthma was determined for 4-year-old a...
Lovasi et al. [1]) document the relationship between the density of
street trees and the prevalence of childhood asthma in New York City.
Their findings suggest street trees are associated with a lower
prevalence, although no causality was inferred. I would like to point out
a number of methodological issues which should benefit future studies on
this subject.
Prevalence of asthma was determined for 4-year-old and 5-year-old
children using data from school screenings in 1999. Street tree density
was derived from the 1995 street tree census completed by the Parks and
Recreation Department of the City of New York and expressed as the total
number of trees on streets segments divided by the land area. Data was
aggregated at the level of United Hospital Fund (UHF) areas. Additional
variables used in the analysis were population density, racial/ethnic
composition and a measure of proximity to pollution sources. The initial
correlation analysis suggested a negative association between street tree
density and prevalence of asthma. However, one of the strongest positive
associations was between street tree density and population density. This
initially appears somewhat counterintuitive, until it is recognized
exactly which types of trees are included in the analysis. The street tree
census conducted by the Parks and Recreation Department of the City of New
York only considered trees along city streets, and trees in parks and open
space are not included. As a result, the street tree density derived by
Lovasi et al. [1] is a substantial underestimate of the actual number
of trees within a UHF area, in particular in areas with large areas of
parks and open space. In fact, Nowak et al. [2] estimate that New York
City has about 5.2 million trees, while the latest street tree census in
2005-2006 counted 592,130 trees [3]. Street trees,
therefore, account only for around 11% of trees within the study area. The
strong correlation between street tree density and population density is
strongly driven by the fact that the total length of streets segments per
unit area increases with population density. Logic suggests that overall
tree density and population density are likely negatively associated since
many parks and open space occur in areas with lower (average) population
density. The pattern in street tree density by UHF areas is therefore a
poor representation of the overall tree density.
Figure 1 below provides an example of a park in Brooklyn adjacent to
a residential area. While numerous trees are visible on the residential
streets, the number of trees in the park far exceeds the number of street
trees. While Figure 1 is not representative for the entire study area, it
illustrates how not including trees in parks and open space presents a
misleading picture of the potential effects of trees on local air quality
in urban areas
Figure 1 Digital orthophoto of a portion of Prospect Park in
Booklyn, New York City adjacent to a residential area.
Source: United States Geological Survey 2006.
The argument could be made that street trees are more relevant than
those in parks and open space since street trees are much closer to the
residential homes. However, Lovasi et al [1] do not make this argument
and instead aggregate all variables at the level of UHFs. This aggregation
does not allow for a determination of street tree density in close
proximity to the residential addresses of asthma cases. If street trees in
close proximity are deemed of greater relevance than trees in parks and
open spaces at greater distances, an individual or street segment level
analysis is required.
A second methodological issue relates to the determination of the
measure of proximity to pollution sources. Relying on the methodology
presented by Maantay [4], Lovasi et al. [1] create uniform distance
buffers around toxic release inventory sites, stationary point sources and
major truck routes and then determine the percentage of each UHF falling
within one or more of these buffers. While the specific distances and
types of sources were derived from the Maantay [4] study, the authors
fail to highlight the many limitations of this approach as detailed at
length in the original study, including the use of single buffer
distances, treating all pollution sources as being similar, and ignoring
cumulative effects from multiple sources. Perhaps more importantly,
Maantay [4] used the individual geocoded residential locations of
asthma hospitalization cases and determined if they fell within a
particular buffer or not. Lovasi et al. [1] instead determine the
prevalence of asthma as a rate based on the number of children within each
UHF and compared this to the percentage of the area of the UHF falling
within one of more of the buffers around the pollution sources, without
considering the proximity of individual cases to pollution sources. The
data aggregation to the level of UHFs represents a very substantial loss
of information. No evidence is presented that aggregation at the level of
UHF areas is justified given the nature of the research question since it
remains unclear at what (spatial) scale the potential effects of street
trees on air quality are expected to occur.
Future research efforts in this area should consider the following
three refinements:
1) Developing a more robust measure of tree density
which includes trees in parks and open spaces. This could be addressed by
using land use or land cover maps supplemented with field sampling as
employed by Nowak et al. [2].
2) Using individual level analysis
instead of aggregation to coarse units. This would involve geocoding
individual address locations of asthma cases and creating individual-level
measures of tree density and proximity to pollution sources, as well as
creating a meaningful sample of non-asthma cases for comparison.
3)
Employing more robust measures of proximity to pollution sources. One
approach to accomplishing this is to use cumulative distribution functions
as employed by Waller et al. [5] and Zandbergen and Chakraborty [6].
While each of these three elements requires considerable effort, they
should contribute to a much improved understanding of the complex
relationships between tree density and asthma prevalence.
Paul Zandbergen
University of New Mexico
Department of Geography
References
1. Lovasi GS, Quin JW, Neckerman KM, Perzanowksi MS Rundle A. 2008.
Children living in areas with more street trees have lower prevalence of
asthma. J Epidemiol Community Health 2008;62:647-649.
2. Nowak DJ, Hoehn III RE, Crane D E, Stevens JC, Walton JT. Assessing
urban forest effects and values, New York City's urban forest. Resource
Bulletin NRS-9. United States Department of Agriculture, Forest Service,
Northern Research Station, 2007.
3. Peper PJ, Mcpherson EG, Simpson JR, Gardner SL, Vargas KE, Xiao Q.
New York City, New York municipal forest resource analysis. Center for
Urban Forest Research, United States Department of Agriculture, Forest
Service, Pacific Southwest Research Station, 2007.
4. Maantay J. Asthma and air pollution in the Bronx: methodological and
data considerations in using GIS for environmental justice and health
research. Health Place 2007;13:32-56
5. Waller LA, Louis TA, Carlin BP. 2007. Environmental justice and
statistical summaries of differences in exposure distributions. J Exposure
Analysis and Env Epi 1999;9:56–65.
6. Zandbergen PA, Chakraborty J. Improving environmental exposure
analysis using cumulative distribution functions and individual geocoding.
Int J Health Geographics 2006;5:23.
Daniel D Reidpath is slightly misguided to observe that social
inequalities in
health have "not yet been elevated to the status of having its own
National
Library of Medicine MeSH (medical subject) heading", and his remark hence
calls for some additional precision.
As a MeSH search for inequalit* will indicate, the National Library
of Medicine
lists "Inequality" and "Inequalities" as entry terms for its
"Soc...
Daniel D Reidpath is slightly misguided to observe that social
inequalities in
health have "not yet been elevated to the status of having its own
National
Library of Medicine MeSH (medical subject) heading", and his remark hence
calls for some additional precision.
As a MeSH search for inequalit* will indicate, the National Library
of Medicine
lists "Inequality" and "Inequalities" as entry terms for its
"Socioeconomic
Factors" heading, which was introduced in 1968. The other MeSH entry for
social factors, namely "Social Environment", does not mention inequalities
in
that respect. Admittedly, these headings do not allow for a clear mapping
of
the health inequalities literature, which is better accessed through user-submitted search strings like "health inequalit*[tw]."
Nevertheless, much more recently, and as a MeSH search for disparit*
indicates, the National Library of Medicine has introduced "Health Status
Disparities" in its topical indexing. The heading coverage is described as
"variation in rates of disease occurrence and disabilities between
socioeconomic and/or geographically defined population groups." A PubMed
search on the heading already returns over 500 references, consistent with
Daniel D Reidpath's view that health inequalities have become a central
element of the research agenda for social epidemiologists, sociologists of
health and illness, and virtually any scholar interested in health
economics
and welfare.
Another new heading introduced in 2008 is "Healthcare Disparities,"
which
covers "Differences in access to or availability of facilities and
services" -- a
partial definition of social inequalities in health, as it is much more
restrictive
in scope and focuses on the single but crucial dimension of access to
health
services. The provision of a specific heading for inequalities in access
to
healthcare, however, comes with several cross-national and cross-sectoral
advantages, and constitutes a valuable bibliographic tool for researchers
in
that respect.
What Daniel D Reidpath's comment underlines is the variety of terms
associated with "social inequalities in health" in international research.
In the
American context, research on the differential distribution of mortality
and
morbidity by socio-economic status (and other social factors) is
susceptible
to be flagged as research on health "disparities" instead of
"inequalities" or
"inequities." Acknowledging another geographical bias, Paul Braveman has
observed that "‘health equity’ is a term rarely encountered in the United
States but more familiar to public health professionals elsewhere." [1].
In
Britain, the political history of health inequalities shows that the more
neutral
terms "health variations" were instrumental in maintaining health
inequalities
on the political agenda, following governmental reluctancy towards the
conclusions of the Black report [2,3].
An explanation for variations in research terminology might relate to
national
contexts of health politics. In the case of the United States, it would be
seemingly unsurprising to observe that a nation that tolerates high levels
of
inequality within its population would prefer the term "disparity" to
address a
phenomenon otherwise addressed as "inequality", a term which would appear
to be politically connoted in the American polity. Existing data on
inequality
and public opinion tend to reveal, however, a more complex picture, in
which
attitudes towards inequality exhibit less cross-national variation than
policy
preferences [4,5].
More generally, research on health inequalities will inevitably
intersect with
other forms of social research, such as racial and ethnic inequality [6].
In fact,
health inequalities are shaped by a large array of factors, not all of
which
should not be expected to be linguistic or rhetorical like the ones
mentioned
here; in France, for instance, institutional factors are constraining the
development of both research and policy regarding health inequalities
[7,8].
Current scholarship, however, has given considerably less attention to the
relationship between health inequalities and institutional variables
derived
from the political context.
This brief response aims not only at rectifying the slight inadequacy
in Daniel
D Reidpath's review, but also at showing how social inequalities in health
call
for interdisciplinary research perspectives in health and society, as
actively
promoted by the JECH. One might finally want to stress the dearth of
political
analysis in this field of research [9].
References
[1] Braveman, P. Health disparities and health equity: concepts and
measurement. Annu Rev Public Health 2006;27:167–94.
[2] Berridge V. Blume S, eds. Poor health. Social inequality before
and after
the Black Report. London: Frank Cass, 2003.
[3] Macintyre S. Before and after the Black report: four fallacies.
In: Berridge V.
Blume S, eds. Poor health. Social inequality before and after the Black
Report.
London: Frank Cass, 2003:198–219.
[4] Pontusson J. Inequality and prosperity in contemporary
capitalism. Ithaca,
NY: Cornell University Press, 2005.
[5] McCall L, Kenworthy L. Americans' social policy preferences in
the era of
rising inequality. Unpublished manuscript, 2008.
[6] Gamble VN, Stone D. US policy on health inequities: the interplay
of
politics and research. J Health Polit Policy Law 2006;31:93–126.
[7] Berthod-Wurmser M. Programmes de recherche et débat public sur
les
inégalités de santé: la France est-elle en retrait ? In: Leclerc A, Fassin
D,
Grandjean H, et al. Les inégalités sociales de santé. Paris: La
Découverte,
2000: 69–80.
[8] Briatte F. Lutter contre les inégalités de santé en France et en
Grande-
Bretagne. [Master's thesis]. Grenoble: Institute of Political Studies,
University
of Grenoble, 2006.
[9] Judge, K. Politics and health: policy design and implementation
are even
more neglected than political values? Eur J Pub Health 2008;18:355–356.
The recent JECH paper by Li et al. (2008) is a valuable contribution
to the literature on the public health impacts and epidemiology of H5N1
avian influenza in humans.
The authors note that both the H5N1 and the 1918 influenza virus
affected young healthy adults more severely than the
1957/1968 pandemic viruses and inter-pandemic influenza viruses, which are
tyically associated with higher mortality among infants...
The recent JECH paper by Li et al. (2008) is a valuable contribution
to the literature on the public health impacts and epidemiology of H5N1
avian influenza in humans.
The authors note that both the H5N1 and the 1918 influenza virus
affected young healthy adults more severely than the
1957/1968 pandemic viruses and inter-pandemic influenza viruses, which are
tyically associated with higher mortality among infants and the elderly,
and noted that mortality from the H5N1 avian influenza and 1918 H1N1 virus
have both been associated with cytokine storm disease presentations.
It is important to note that although there appear to be marked
parallels in the clinical presentations of fatal cases of the H5N1 bird
flu and 1918 Spanish flu, there are significant differences in age-specific mortality profiles for these two viruses.
The peak morbidity/mortality among confirmed human cases of the H5N1
bird flu occurs among adolescents and young adults in the 10-30 year old
cohort, while peak mortality from the 1918 H1N1 Spanish influenza was
concentrated among infants, the elderly, and individuals in the 25-35 year
age range (Taubenberger and Morenz 2006; Murray et al. 2006). This can be
readily discerned by comparing H5N1 age-specific morbidity/mortality rates
presented in WHO-PRO (2007), with age-specific excess mortality rate charts
for 1918-1919 Spanish Flu presented in Taubenberger & Morens (2006),
and Murray et al. (2006).
This observed difference in age-specific mortality rates is
particularly significant in view of the epidemiological impacts at the
population level in developing countries, where there are higher relative
and absolute numbers of individuals within younger age cohorts, and where
local public health infrastructures have less capacity and fewer resources
to cope with infectious disease epidemics and influenza pandemics.
References
Murray, C.J.L., A. D. Lopez, B. Chin, D. Feehan, K.H. Hill. 2006.
Estimation of potential global pandemic infl uenza mortality on the basis
of vital registry data from the 1918–20 pandemic: a quantitative analysis.
Lancet 368: 2211–2218.
Taubenberger, J. K, and D. Morens. 2006. 1918 Influenza: the mother
of all pandemics. Emerging Infectious Diseases 12:15-22. URL:
http://www.cdc.gov/ncidod/EID/vol12no01/05-0979.htm
World Health Organization - Pacific Regional Office. 2007. Avian
influenza A(H5N1) cases by age group and outcome (as of 10 September
2007). World Health Organization Regional Office for Western Pacific,
Manila, Philippines. URL:
http://www.wpro.who.int/NR/rdonlyres/FD4AC2FD-B7C8-4A13-A32C-
6CF328A0C036/0/Slide4.jpg
I enjoyed this well observed article. I wonder if there is a simpler
distinction we could make.
When we prevent a case of tetanus or polio or other infection then
that illness never occurs.
When we are talking about "preventing" the chronic degenerative
illnesses such as IHD and stroke we are probably not preventing them
entirely. We are usually postponing the onset of their ill effects so...
I enjoyed this well observed article. I wonder if there is a simpler
distinction we could make.
When we prevent a case of tetanus or polio or other infection then
that illness never occurs.
When we are talking about "preventing" the chronic degenerative
illnesses such as IHD and stroke we are probably not preventing them
entirely. We are usually postponing the onset of their ill effects so that
people either die of something else, or at least get more years of life in
good health. These are worthwhile goals, but the postponement of morbidity
and mortality is not the same as preventing them.
And no matter how good our postponing we none of us can postpone all
illness for ever.
“A Novel Hypothesis to Explain Associations of Carbon Monoxide and
Nitrogen Dioxide with Deaths from Respiratory Disease”
Dear Editor:
I am writing to comment on the article[1] entitled “Atmospheric
pollutants and mortalities in English local authority areas” by E. G.
Knox. The paper analyzed a large body of epidemiologic data linking
various forms of air pollution to the death rates from several dise...
“A Novel Hypothesis to Explain Associations of Carbon Monoxide and
Nitrogen Dioxide with Deaths from Respiratory Disease”
Dear Editor:
I am writing to comment on the article[1] entitled “Atmospheric
pollutants and mortalities in English local authority areas” by E. G.
Knox. The paper analyzed a large body of epidemiologic data linking
various forms of air pollution to the death rates from several diseases,
including pneumonia, COPD, and lung cancer.
I want to suggest that in some cases the author unknowingly mis-classified the exposure, and that the associations with carbon monoxide
(CO) and nitrogen dioxide (NO2) may be more plausibly linked to an
unsuspected exhaust component of engines, namely, methyl nitrite (MN).
The paper does not give any information on the actual ambient
concentrations of any of the pollutants, it presents only the results of
a correlation analysis between death rates and pollutant concentrations.
That is unfortunate, because at least for CO and NO2 there are many other
studies in England that indicate that the levels of those two pollutants
are far below the levels known to have any harmful health effects.
Carslaw[2] published a recent study of CO concentration near Marylebone
Road, which is a major arterial road located
in central London, and found that mean CO concentrations dropped from
2.1mg/m3 (approximately 2 ppm) in 1998 down to 0.8 mg/m3 in 2005. Another
study[3] found that, depending on wind speed, the CO concentration in
Manchester varied from 0.4 to 1.12 ppm. The same study found that NOx
concentrations varied from 24 to 79 ppb
in Manchester, from 34 to 55 ppb in Edinburgh, and from 7 to 31 ppb in
Birmingham.
The toxicology of CO is very well known to alter oxygen saturation
in red blood cells, but only at concentrations that are far above the
those observed in England during the time period 1996-2004. Exposure to
CO at the current criterion concentration (9 ppm) produces[4]
carboxyhemoglobin (CoHg ) of only about 1.4-2.0%, which is clinically
insignificant (and only slightly above the endogenous levels of CoHg).
Thom[5] has demonstrated that CO can have more subtle biological effects
that he thinks can be significant in cases of frank CO poisoning.
However, his in vivo studies with rats involved CO concentrations of 1000
ppm and above. In one animal study[5] he found no significant effects at
concentrations below 100 ppm.
Regarding attributing deaths from lung diseases to ambient CO, a
remarkable development is the recent interest in using CO as a therapeutic
agent for lung disease. One recent review[6] cited 159 references, with many
studies indicating that the gas can produce a variety of useful
therapeutic effects, including anti-inflammatory, anti-proliferative, and
vasodilation. Brief animal exposures of 250 ppm of CO protected against
ventilator-induced lung injury and reduced the asthmatic response to
allergens[7]. It also reduced mortality in an animal model of pneumonia[8].
One clinical trial[9] of patients with COPD using CO exposure of 125 ppm
demonstrated a reduction in sputum eosinophils and in response to
methacholine challenge.
Hence I find it less than plausible that the very low ambient levels
of CO in England could be the direct cause of so many deaths from
respiratory disease.
I want to present an alternative hypothesis to explain these
pollutant-mortality correlation results. I have argued[10] [11] that the use
of methyl ether (such as MTBE or TAME) in gasoline creates MN in the
exhaust. Since CO is primarily an engine exhaust product, increased CO
would be expected to be strongly correlated with MN exhaust. Dr. Knox
stated: “Engine exhaust accounts for the greater part of carbon monoxide,
... and nitrogen oxides...” Furthermore, MN can easily be confounded with
NO2, as I have argued previously (Occ & Env Med 2008, in press). One
review[12] stated: ”The overall results suggest that outdoor NO2“. was serving
as a marker for more causal airborne agents rather than a direct effect of
NO2“. A more detailed analysis of this confounding effect, based on many
previously published studies of the epidemiology of NO2, is currently in
preparation. Another review[11] indicated that the alkyl nitrites are known
to be harmful to both the respiratory and immune systems, and MN has been
shown[13] to be mutagenic by the Ames test.
While I feel that this MN hypothesis is extremely plausible (and
especially more plausible than that the effects are directly due to CO and
NO2), until such time as MN is positively identified its role in
environmental epidemiology remains tentative. We need a careful study of
the presence of MN in engine exhaust using the techniques of gas-phase
analytical chemistry. However, I (personally) have neither the equipment
nor expertise for such studies. I can only urge that those with such
expertise investigate this issue.
Sincerely
Professor Peter M. Joseph, Ph.D.
School of Medicine
University of Pennsylvania
Philadelphia, PA, USA
email = joseph@rad.upenn.edu
I have no competing interests.
References
1. Knox EG. Atmospheric pollutants and mortalities in English local
authority areas. J Epidemiol Community Health 2008;62(5):442-7.
2. Carslaw DC, Beevers SD, Tate JE. Modelling and assessing trends in
traffic-related emissions using a generalised additive modelling approach.
Atmospheric Environment 2007;41(26):5289-5299.
3. Longley ID, Inglis DWF, Gallagher MW, Williams PI, Allan JD, Coe
H. Using NOx and CO monitoring data to indicate fine aerosol number
concentrations and emission factors in three UK conurbations. Atmospheric
Environment 2005;39(28):5157-5169.
4. Utell MJ, Warren J, Sawyer RF. Public health risks from motor
vehicle emissions. Annu Rev Public Health 1994;15:157-78.
5. Thom SR, Fisher D, Xu YA, Garner S, Ischiropoulos H. Role of
nitric oxide-derived oxidants in vascular injury from carbon monoxide in
the rat. Am J Physiol 1999;276(3 Pt 2):H984-92.
6. Hoetzel A, Schmidt R. Kohlenmonoxid--Gift oder potenzielles
Therapeutikum? Anaesthesist 2006;55(10):1068-79.
7. Ryter SW, Choi AM. Therapeutic applications of carbon monoxide in
lung disease. Curr Opin Pharmacol 2006;6(3):257-62.
8. Hoetzel A, Dolinay T, Schmidt R, Choi AM, Ryter SW. Carbon
monoxide in sepsis. Antioxid Redox Signal 2007;9(11):2013-26.
9. Bathoorn E, Slebos DJ, Postma DS, Koeter GH, van Oosterhout AJ,
van der Toorn M, et al. Anti-inflammatory effects of inhaled carbon
monoxide in patients with COPD: a pilot study. Eur Respir J
2007;30(6):1131-7.
10. Evidence for methyl nitrite as an exhaust component from engines
with certain fuels. Annual Meeting Proceedings CD-ROM Air & Waste
Management Association, 99th, New Orleans, LA, June 20-23, 2006; 2006; New
Orleans, LA.
11. Joseph PM. Paradoxical ozone associations could be due to methyl
nitrite from combustion of methyl ethers or esters in engine fuels.
Environ Int 2007;33(8):1090-106.
12. Delfino RJ. Epidemiologic evidence for asthma and exposure to air
toxics: linkages between occupational, indoor, and community air pollution
research. Environ Health Perspect 2002;110 Suppl 4:573-89.
13. Tornqvist M, Rannug U, Jonsson A, Ehrenberg L. Mutagenicity of
methyl nitrite in Salmonella typhimurium. Mutat Res 1983;117(1-2):47-54.
A recent article in your journal from Caerphilly study demonstrates
that increasing consumption of milk helps control metabolic syndrome, a
known risk factor for ischemic cerebro vascular accident (CVA) [1].
Previous studies have demonstrated that milk also helps control
hypertension, another major risk factor for ischemic CVA [2].A long term
Japanese study of men between ages of 55-68 years demonstr...
A recent article in your journal from Caerphilly study demonstrates
that increasing consumption of milk helps control metabolic syndrome, a
known risk factor for ischemic cerebro vascular accident (CVA) [1].
Previous studies have demonstrated that milk also helps control
hypertension, another major risk factor for ischemic CVA [2].A long term
Japanese study of men between ages of 55-68 years demonstrated that men
who consumed 16 ounces or more milk per day cut down their risk of stroke
to half compared to the men who did not drink milk.[3]. This study also
indicated that calcium from non-dairy intake did not reduce the risk of
stroke. Another prospective study of 53000 Japanese men and women found
that total calcium intake and calcium from dairy products were associated
with reduced mortality from stroke.[4] Nurses’ health study of more than
85000 US women aged 35 to 59 years have indicated that women who consumed
higher calcium, especially dairy calcium, lowered their risk of ischemic
CVA. [5]The Caerphilly Cohort Study, which followed a group of 2403 men
aged 45 to 59 years for 20 to 24 years, demonstrated that men who drank
two cups or more milk per day had lower risk of ischemic CVA compared to
the men who did not drink milk. [2] Milk reduced that risk even further in
patients who already had known atherosclerotic disease [2]. Authors of
this study pooled the data of 10 cohort studies on this subject and
concluded that milk drinking may be associated with small but worthwhile
reduction of stroke risk[2].
In spite of these studies, none of the dietary recommendation specifically
asks general public or stroke patients to increase the consumption of milk
to reduce their future risk of stroke. In light of these studies,
consideration should be given to change those recommendations or at least
carry out further studies to address that question.
References
1. Elwood PC, Pickering JE, Fehily AM: Milk and dairy consumption,
diabetes and the metabolic syndrome: the Caerphilly prospective study, J
Epidemiol Community Health; , Aug; 61(8) 695-8,2007
2. Miller GD, Jarvis JK, McBean LD: Handbook of dairy foods and
nutrition: CRC press Boca Raton 2007 page 99-139,75-78, 70
3. Abbot, RD et al; Effect of dietary calcium and milk consumption on
risk of thromboembolic stroke in older middle aged men. The Honolulu Heart
Program. Stroke, 27, 813,1996
4. Umesawa, M et al ; Dietary intake of calcium in relation to
mortality from cardiovascular disease , the JACC study ,Stroke 37, 20,
2006
5. Iso, H et al, Prospective study of calcium, potassium and magnesium
intake and risk of stroke in women, Sroke 30, 1772,1999
In this issue of the journal, a study by Christensen et al. reported
on how the social gradient in long-term sickness was explained by a number
of risk factors related to work environment and health behavior in a
sample of Danish employees.[1]
I agree with Christensen et al. that it is important to examine what
mediates (or explains) social gradients in health: Not only from a
scholarly inter...
In this issue of the journal, a study by Christensen et al. reported
on how the social gradient in long-term sickness was explained by a number
of risk factors related to work environment and health behavior in a
sample of Danish employees.[1]
I agree with Christensen et al. that it is important to examine what
mediates (or explains) social gradients in health: Not only from a
scholarly interest in etiology, but also because interventions targeted at
mediators (e.g. work environment) are more realistic than manipulating the
determinants (e.g. socioeconomic position). Some authors seem to suggest
that mediation is not a tractable problem, but I think that Christensen et
al. should be applauded for this contribution.[2]
Christensen et al report that controlling for health behavior and
work environment reduced the sickness absence rate ratios by 22–57%. The
percentages were arrived at by comparing the regression coefficients
before and after control for health behavior and work environment. If
Christensen et al had used a linear regression model with a continuous and
normally distributed dependent variable the difference in coefficients
could have been used to calculate the percentage explained. However, as
the study by Christensen et al. uses Poisson regression the difference in
coefficients does not consistently estimate the proportion of the
association explained by health behavior and work environment because the
two regression models that are compared are nonlinear. The bias might be
small, but this depends on the actual data used by Christensen et al. as
shown in simulation studies.[3][4]
Christensen et al. use change in rate ratios - a relative measure of
association - to capture the effect of intermediary variables on the
social gradient in sickness absence. For example, the authors report only
a small reduction of 13% (from 4.22 to 3.66) in the rate ratio between the
group of executive managers/academics and the group of semiskilled and
unskilled workers when controlling for health behavior. This suggests that
regardless of whether we looked at employees with a ‘healthy’ health
behavior or those with an ‘unhealthy’ health behavior, the semiskilled and
unskilled workers would still have a 3.66 times higher rate of sickness
absence. Among the ‘healthy’ employees the two rates would likely be much
closer in absolute terms than among the ‘unhealthy’ even though the rate
ratio is 3.66 regardless of health behavior. So, among the ‘healthy’ the
(absolute) rate difference between executive managers/academics and
semiskilled and unskilled workers might be quite small even though the
rate ratio is high simply because the rates are low among the 'healthy'
(my argument is borrowed from a study by Lynch et al. published in an
earlier version of this journal[5]). I think that the authors’ analysis
and interpretation is perfectly correct, but I think that it is open to
debate if relative inequalities – when the risk or rates are small - are
as important as a public health problem as absolute inequalities.
I want to stress that the paper by Christensen et al. is by no means
a faulty paper. The points that I have raised are minor and are not meant
to discredit the work of Christensen et al.
References
1. Christensen C.B., Labriola M, Lund T et al. Explaining the social
gradient in long-term sickness absence: a prospective study of Danish
employees. J Epidemiol Community Health 2008;181-3.
2. Kaufman JS, MacLehose RF, Kaufman S. A further critique of the
analytic strategy of adjusting for covariates to identify biologic
mediation. Epidemiol Perspect Innov 2004;1:4.
3. Ditlevsen S, Christensen U, Lynch J et al. The mediation
proportion: a structural equation approach for estimating the proportion
of exposure effect on outcome explained by an intermediate variable.
Epidemiology 2005;16:114-20.
4. Mackinnon DP, Lockwood CM, Brown CH et al. The intermediate
endpoint effect in logistic and probit regression. Clin Trials 2007;4:499-
513.
5. Lynch J, Davey SG, Harper S et al. Explaining the social gradient
in coronary heart disease: comparing relative and absolute risk
approaches. J Epidemiol Community Health 2006;60:436-41.
Thank you for your review of my recently published book "Social
Epidemiology - Strategies for Public Health Activism". You raise the
question of how social epidemiologists can find "strategies to put social
epidemiological findings into practice". In Chapter 9, pages 273-309,
readers of the book will find a comprehensive review entitled "Theories
for Social Epidemiological Interventions"...
Thank you for your review of my recently published book "Social
Epidemiology - Strategies for Public Health Activism". You raise the
question of how social epidemiologists can find "strategies to put social
epidemiological findings into practice". In Chapter 9, pages 273-309,
readers of the book will find a comprehensive review entitled "Theories
for Social Epidemiological Interventions" including: behavioral
modification, social learning theory, the Health Belief Model, the Model
of Behavioral Intentions, meta-analysis, the Transtheoretical Model,
interventions in stress and coping, social marketing, media advocacy,
participatory action research, empowerment interventions, and community
interventions and evaluation. It appears that you overlooked this section
of the book where the answers to your question can be found.
To the editors, the book review title states that I "EDITED" the book
when the book is a single author book by me alone.
It was with great interest that I read the recent article by
Henderson et al.,[1] as my main interests are closely related to the
potential effects of alcohol consumption (and that of other drugs) during
pregnancy. However, although I agree that some of the issues they raise
are relevant, there are several aspects of this article [1] that concern me,
about which I would like to offer some reflection...
It was with great interest that I read the recent article by
Henderson et al.,[1] as my main interests are closely related to the
potential effects of alcohol consumption (and that of other drugs) during
pregnancy. However, although I agree that some of the issues they raise
are relevant, there are several aspects of this article [1] that concern me,
about which I would like to offer some reflections.
First of all, I think that some caution should be exerted when
considering the conclusions made by evaluating observational studies with
different designs, and on different populations. Particularly, if they are
focused on such a complex issue as the potential effects of alcohol
consumption during pregnancy and more specifically, binge-drinking.
Indeed, some inconsistency in the results would be expected from such
studies a priori due to:
a) The heterogeneity of the different studies, either in terms of sample
size and methodological approaches, or in the life styles and genetic
background of the different populations studied.
b) The periods during pregnancy in which exposure occurred, and the
difficulties in determining the exact time. This is particularly important
for those mothers that recognized having had any binge-drinking.
c) The differing amount of alcohol intakes [2], and the difficulties to
define the exact amount, that may also be more marked in some populations
than in others.
d) The genetic constitutions of the populations studied. In this sense,
there are studies demonstrating that polymorphic mutations of a single
nucleotide diminish the individual metabolism of alcohol [3], and that the
frequencies of different polymorphisms vary between the human populations
[4-5]. Hence, this genomic variability and metabolic susceptibility either
in the women or in the embryo may result in different risks for congenital
defects. In addition, the huge amount of information provided by the
molecular analyses of the human genome has highlighted the impressive
complexity in the structural and functional aspects of DNA [6-11]. This
complexity also affects the relationship between functional polymorphic
variants of DNA, and the individual susceptibility to the effects of
different exposures, as well as the presence/absence of some particular
congenital defects.
Additionally, and considering all the above commented aspects, it is
not surprising that different epidemiological studies may produce
different results, even if they are well designed in epidemiological terms
and they have been “filtered for the high sensitivity filter”. Thus,
inconsistencies should not always be interpreted as only being due to
methodological aspects. Moreover, I consider that the results of
epidemiological analyses on the potential teratogenic effects of different
maternal exposures, should be evaluated not only through the statistical
significance of the results, but in the light of their current biological
bases, as well as evaluating the maternal benefit versus the embryonic-
fetal risk, before reaching any conclusion.
Finally, and although Henderson et al.[1] make general comments on
some of these particular aspects, in their conclusion they state that “In
the absence of a strong research base on which to make any strong clinical
recommendations… despite the concurrent lack of evidence, from a public
health point of view we would suggest that it may be worthwhile
recommending pregnant women to avoid binge-drinking during pregnancy.” I
totally disagree with this recommendation, essentially on the basis of
three issues. First, making reference to avoid binge-drinking after the
first sentence may give rise to the idea that lower doses of alcohol might
be safe. Second, by recommending that the use of alcohol should be avoided
during pregnancy could be interpreted that alcohol consumption should
cease once women know that they are pregnant. However, when a mother
realizes that she is pregnant, nearly all the future organs and systems in
the fetus have been formed. I consider it more appropriate to recommend to
all woman who plan to becoming pregnant that they should avoid alcohol
before abandoning contraception. Third, in spite of that the results of
the observational studies are not consistent or are at times
contradictory, and given that the effects of alcohol in animals cannot be
fully extrapolated to humans, we must bear in mind that this exposure to
alcohol is totally unnecessary. Hence, even if the possibility of having
an adverse effect were remote, and even if the risks were only for women
having a particular genomic susceptibility, in the absence of a biological
test for susceptibility the embryo-foetal risk is valuable, Thus, the only
effective and correct recommendation from either the clinical or public
health point of view is that of total abstention in women who could become
pregnant and indeed, before they become pregnant. Other recommendations
for this unnecessary exposure may be tragic for some women and thus, for
individual and public health.
María Luisa Martínez-Frías
- ECEMC, Centro de Investigación sobre Anomalías Congénitas (CIAC),
Instituto de Salud Carlos III, Ministerio de Sanidad y Consumo, Madrid
(Spain).
- Centre for Biomedical Research on Rare Diseases (CIBERER), Madrid
(Spain).
- Departamento de Farmacología, Facultad de Medicina, Universidad
Complutense, Madrid (Spain).
Address Correspondence to: Dr. María Luisa Martínez-Frías, Centro de
Investigación sobre Anomalías Congénitas (CIAC), Instituto de Salud Carlos
III, Sinesio Delgado 4-6, 28029, Madrid, Spain.
References
1. Henderson J, Kesmodel U, Gray R. Systematic review of the fetal
effects of prenatal binge-drinking. J Epidemiol Community Health.
2007;61:1069-1073.
2. Martínez-Frias ML, Postmarketing analysis of medicines: methodology and
value of the spanish case-control study and surveillance system in
preventing birth defects. Drug Saf. 2007;30(4):307-16. Review.
3. Liu QR, Drgon T, Walther D, Johnson C, Poleskaya O, Hess J, Uhl GR.
Pooled association genome scanning: validation and use to identify
addiction vulnerability loci in two samples. Proc Natl Acad Sci U S A.
2005 Aug 16;102(33):11864-9. Rao VR, Bhaskar LV, Annapurna C, Reddy AG,
Thangaraj K, Rao AP, Singh L. Single nucleotide polymorphisms in alcohol
dehydrogenase genes among some Indian populations. Am J Hum Biol. 2007 May
-Jun;19(3):338-44.
4. Osier MV, Pakstis AJ, Soodyall H, Comas D, Goldman D, Odunsi A,
Okonofua F, Parnas J, Schulz LO, Bertranpetit J, Bonne-Tamir B, Lu RB,
Kidd JR, Kidd KK. A global perspective on genetic variation at the ADH
genes reveals unusual patterns of linkage disequilibrium and diversity. Am
J Hum Genet. 2002 Jul;71(1):84-99.
5. Sebat J, Lakshmi B, Troge J, Alexander J, Young J, Lundin P, Maner S,
Massa H, Walker M, Chi M, Navin N, Lucito R, Healy J, Hicks J, Ye K,
Reiner A, Gilliam TC, Trask B, Patterson N, Zetterberg A, Wigler M. Large-
scale copy number polymorphism in the human genome. Science. 2004;305:525-
528.
6. Iafrate AJ, Feuk L, Rivera MN, Listewnik ML, Donahoe PK, Qi Y, Scherer
SW, Lee C. Detection of large-scale variation in the human genome. Nat
Genet. 2004;36:949-951.
7. Freeman JL, Perry GH, Feuk L, Redon R, McCarroll SA, Altshuler DM,
Aburatani H, Jones KW, Tyler-Smith C, Hurles ME, Carter NP, Scherer SW,
Lee C. Copy number variation: new insights in genome diversity. Genome
Res. 2006;16:949-961.
8. Stranger BE, Forrest MS, Dunning M, Ingle CE, Beazley C, Thorne N,
Redon R, Bird CP, de Grassi A, Lee C, Tyler-Smith C, Carter N, Scherer SW,
Tavare S, Deloukas P, Hurles ME, Dermitzakis ET. Relative impact of
nucleotide and copy number variation on gene expression phenotypes.
Science. 2007;315:848-853.
9. Kapranov P, Cheng J, Dike S, Nix DA, Duttagupta R, Willingham AT,
Stadler PF, Hertel J, Hackermuller J, Hofacker IL, Bell I, Cheung E,
Drenkow J, Dumais E, Patel S, Helt G, Ganesh M, Ghosh S, Piccolboni A,
Sementchenko V, Tammana H, Gingeras TR. Genome-wide RNA maps reveal new
RNA classes and a possible function for pervasive transcription. Science.
2007;316:1484-1488.
10. The ENCODE Project Consorcium. Identification and analysis of
functional elements in 1% of the human genome by the ENCODE pilot project.
Nature 2007;447:799-816.
11. Martínez-Frías ML, The human genome. An extremely complex system.Bol
ECEMC Rev Dismorf Epidemiol 2007;82-
91.(http://bvs.isciii.es/mono/pdf/CIAC_06.pdf)
The interesting paper of Dr Bellis and colleagues [1] reports
strikingly increased mortality in rock and pop stars.
A widespread opinion is that fame is the reason for the manifold
psychological problems of the stars. These problems are seen as a
consequence of the pressure of the fans, the media, the music industry, or
obtrusive paparazzi. Also, the availability of drugs and alcohol and the
problem of...
The interesting paper of Dr Bellis and colleagues [1] reports
strikingly increased mortality in rock and pop stars.
A widespread opinion is that fame is the reason for the manifold
psychological problems of the stars. These problems are seen as a
consequence of the pressure of the fans, the media, the music industry, or
obtrusive paparazzi. Also, the availability of drugs and alcohol and the
problem of coping with obscurity after a period of fame are commonly
stressed as etiological factors.
The crucial question is, however, whether fame leads to psychiatric
problems or – the other way around – certain psychiatric problems may be a
prerequisite for getting famous.
An analysis of the biographies of pop stars who died young showed that
features of personality disorders were present before these stars got
famous.[2]
The main reasons for premature death identified in the study were drug or
alcohol overdose and/or chronic substance abuse. But also some other
reasons for increased mortality, such as suicide, accidents and violence,
point into the direction of a certain psychiatric illness: The features of
borderline personality disorder include substance abuse, impulsive
behaviour, high-risk behaviour (e.g. speeding), depression, suicidality,
self-mutilation (mostly in women), unsteady interpersonal relationships,
problems with sexuality, feelings of emptiness, and eating disorders.
Etiological factors include traumatic childhood experiences and genetic
contributions.
In most studies with borderline patients, the mean age is around 27 years,
which may be a possible explanation for the magic age of 27 at which
Joplin, Hendrix, Morrison and Cobain died.
Since Aristotle, who saw the association between melancholia and poetry,
many scientific authors have investigated the relationship of “genius and
madness”. A number of studies found significantly increased rates of
psychiatric disorders in artists, in particular in performance artists
(e.g. singers and actors).[3-5]
The striking relationship between death, drugs, and Rock ‘n’ Roll may be
explained by the dopamine reward system and the associated endogenous
opioid system of the human brain. Borderline patients seem to have a
dysfunction of these systems, which they try to compensate by using heroin
and cocaine, drugs that stimulate these systems directly. Also, frequent
sexual contacts, risky behaviours, aggression, self-mutilation or
overeating increase endorphin levels, but one of the best techniques is to
get attention by a large audience. Narcissism is one of the main features
of borderline personality disorder, and this explains why the affected
persons try harder to get famous and develop more creativity and fantasy
as musicians, actors or writers. Due to their high emotionality, their
performance is perceived as more touching and authentic by the public.
Should we warn persons at risk to get famous? The answer is no. Performing
on stage may be a more successful therapy than any psychiatric treatment,
and without these exceptional artists, our culture would suffer great
losses.
Prof. Dr. B. Bandelow
Department of Psychiatry and Psychotherapy
University of Göttingen
von-Siebold-Str. 5
D-37085 Göttingen, Germany
Tel. +49-551-396607
Fax +49-551-398952
E-mail: Sekretariat.Bandelow@medizin.uni-goettingen.de
References
1. Bellis M, Hennell T, Lushey C, Hughes K, Tocque K, Ashton J. Elvis
to Eminem: quantifying the price of fame though early mortality of
European and North American rock and pop stars. J Epidemiol Community
Health 2007;2007(61):896-901.
2. Bandelow B. Celebrities - vom schwierigen Glück, berühmt zu sein
[Celebrities - About the difficult luck to be famous]. 2nd edition.
Reinbek, Germany: Rowohlt; 2006.
3. Andreasen NC. Creativity and mental illness: prevalence rates in
writers and their first-degree relatives. American Journal of Psychiatry.
1987;144(10):1288-92.
4. Ludwig AM. Creative achievement and psychopathology: comparison among
professions. American Journal of Psychotherapy. 1992;46(3):330-56.
5. Post F. Creativity and psychopathology. A study of 291 world-famous
men. Br J Psychiatry. 1994;165(2):22-34.
Lovasi et al. [1]) document the relationship between the density of street trees and the prevalence of childhood asthma in New York City. Their findings suggest street trees are associated with a lower prevalence, although no causality was inferred. I would like to point out a number of methodological issues which should benefit future studies on this subject.
Prevalence of asthma was determined for 4-year-old a...
Daniel D Reidpath is slightly misguided to observe that social inequalities in health have "not yet been elevated to the status of having its own National Library of Medicine MeSH (medical subject) heading", and his remark hence calls for some additional precision.
As a MeSH search for inequalit* will indicate, the National Library of Medicine lists "Inequality" and "Inequalities" as entry terms for its "Soc...
The recent JECH paper by Li et al. (2008) is a valuable contribution to the literature on the public health impacts and epidemiology of H5N1 avian influenza in humans.
The authors note that both the H5N1 and the 1918 influenza virus affected young healthy adults more severely than the 1957/1968 pandemic viruses and inter-pandemic influenza viruses, which are tyically associated with higher mortality among infants...
Sir
I enjoyed this well observed article. I wonder if there is a simpler distinction we could make.
When we prevent a case of tetanus or polio or other infection then that illness never occurs.
When we are talking about "preventing" the chronic degenerative illnesses such as IHD and stroke we are probably not preventing them entirely. We are usually postponing the onset of their ill effects so...
“A Novel Hypothesis to Explain Associations of Carbon Monoxide and Nitrogen Dioxide with Deaths from Respiratory Disease”
Dear Editor:
I am writing to comment on the article[1] entitled “Atmospheric pollutants and mortalities in English local authority areas” by E. G. Knox. The paper analyzed a large body of epidemiologic data linking various forms of air pollution to the death rates from several dise...
Dear Editor
A recent article in your journal from Caerphilly study demonstrates that increasing consumption of milk helps control metabolic syndrome, a known risk factor for ischemic cerebro vascular accident (CVA) [1]. Previous studies have demonstrated that milk also helps control hypertension, another major risk factor for ischemic CVA [2].A long term Japanese study of men between ages of 55-68 years demonstr...
Dear Editor
In this issue of the journal, a study by Christensen et al. reported on how the social gradient in long-term sickness was explained by a number of risk factors related to work environment and health behavior in a sample of Danish employees.[1]
I agree with Christensen et al. that it is important to examine what mediates (or explains) social gradients in health: Not only from a scholarly inter...
Dear Dr. van Lenthe,
Thank you for your review of my recently published book "Social Epidemiology - Strategies for Public Health Activism". You raise the question of how social epidemiologists can find "strategies to put social epidemiological findings into practice". In Chapter 9, pages 273-309, readers of the book will find a comprehensive review entitled "Theories for Social Epidemiological Interventions"...
Dear Editor,
It was with great interest that I read the recent article by Henderson et al.,[1] as my main interests are closely related to the potential effects of alcohol consumption (and that of other drugs) during pregnancy. However, although I agree that some of the issues they raise are relevant, there are several aspects of this article [1] that concern me, about which I would like to offer some reflection...
Dear Editor
The interesting paper of Dr Bellis and colleagues [1] reports strikingly increased mortality in rock and pop stars. A widespread opinion is that fame is the reason for the manifold psychological problems of the stars. These problems are seen as a consequence of the pressure of the fans, the media, the music industry, or obtrusive paparazzi. Also, the availability of drugs and alcohol and the problem of...
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