Comment
Beyond silicosis, is the world failing on silica hazards?
Collis and Yule1 stated in 1933, that “silica is such a body
poison as is lead, even though it exerts its maleficent
influence, especially with regard to tuberculosis,
mainly on the respiratory organs, through which it
gains access to the body”. This statement invites us to
question the editorial2 entitled “The world is failing on
silicosis” in The Lancet Respiratory Medicine. As clinicians,
radiologists, toxicologists, and social scientists working
on health hazards related to crystalline silica exposure,
we delve beyond silicosis, to learn of other dangers
associated with silica.
Collis and Yule’s work directly connects to more
recent research that has been questioning the role of
crystalline silica exposure for the past 20 years, not
only in silicosis but also in diseases still considered
idiopathic (eg connective tissue diseases, pulmonary
alveolar proteinosis, and, as is also discussed, sarcoidosis
and idiopathic pulmonary fibrosis). These diseases are
mainly considered to be of unknown origin, probably
partly because the prevalence of the idea that there is
a single cause for a single disease hinders the thinking
of multiple causes. This limited thinking includes
diseases described as having varied prognoses and
clinical characteristics. An outbreak of autoimmune
disorders in workers with silicosis who were exposed
to high crystalline silica content dusts warned us
against the emergence of new sources of silica hazards.3
During the past 20 years, analogous situations have
supported an association between silica exposure,
silicosis, and other so-called idiopathic diseases.4 The
unprecedented dynamic in therapeutic research on
these disorders should now go hand in hand with
research on their causes, especially when prevention
is possible. Moreover, a sociological and historical
analysis can highlight how fragile and contentious the
aetiological foundation for some diseases has been. It
is thus necessary to develop an agnotological approach5
(ie, to study not only the production of knowledge but
also the mechanisms by which doubt is produced about
scientific evidence).
The founding definition of silicosis, formulated during
the international conference co-organised in 1930 in
Johannesburg by the International Labour Organisation
and the Transvaal Chamber of Mines (a powerful
South African employers’ trade union), narrowed
www.thelancet.com/respiratory Vol 7 August 2019 649
the scope of health surveillance. This definition
reduced the number of diseases assessed to be caused
by crystalline silica inhalation to silicosis, and the
Dirk Wiersma/Science Photo Library
number of occupational contexts of interest to mining
activities (and secondarily to some other occupations
such as stonecutting). Exposure to dust in farming
or building activities were thus mostly forgotten in
medical practice, research, and teachings, as well as
prevention campaigns. The diagnostic boundaries of
silicosis itself were also reduced, by excluding early Published Online
May 17, 2019
stages of the disease caused by silica in the lungs or in http://dx.doi.org/10.1016/
other organs.6 Further research into the causes has thus S2213-2600(19)30174-2
neglected the possible role of silica (and some other
inorganic particles) in several diseases, especially other
granulomatous diseases such as sarcoidosis.
The narrow limits of thinking on silica hazards have
also created inconsistencies in rules for compensation.
For instance, systemic lupus can be compensated
as an occupational disease in the French agricultural
compensation scheme, but is not admissible for salaried
workers in non-agricultural work. Although crystalline
silica was classified as a group 1 carcinogen by the
International Agency for Research on Cancer in 1997,7
the manufacturing processes involving this airborne
contaminant were recognised as such only in 2017 by
the EU.8 In the meantime, industry has been reluctant to
recognise this toxicity.9 These medicolegal and financial
motives explain why education on silica hazards and
compensation rules must not be limited to workers and
employers, but widely taught in the physicians’ primary
and ongoing training.
The question is not do we need more evidence on
silica hazards, but what kind of evidence is missing? As
claimed in the editorial,2 robust epidemiological data
are definitely needed. Nevertheless, silica hazards have
in many respects already been described. Consequently,
efforts must also be made to better understand the
pathogenesis of silica-associated diseases, to discover
the precise cellular targets and inflammatory pathways
linking silica, fibrosis, inflammation, and auto-immunity.
Deciphering the natural history of silica-associated lung
diseases, beyond silicosis, might also help to better
define the classification they encompass. A 2019 study10
has highlighted the high prognostic value of mediastinal
lymphadenopathy on CT-scans in all-cause interstitial
 Comment
lung diseases, but without mentioning the possible
causative role of mineral dust exposures in these
mediastinal lymph nodes. An updated definition and
more refined CT-scan description of the effects of silica,
discussing isolated mediastinal lymphadenopathies as
an early sign of silica exposure, could therefore also help
to evaluate the actual prevalence of silica hazards.
Beyond pathogenesis and imaging considerations,
broadening our view of silicosis will also aid under­
standing as to how a high prevalence of communicable
diseases can coexist with high mineral dust exposures
in some African countries that contradict the
epidemiological transition model. Silica hazards must
be addressed through a socioecological approach,11
embracing working conditions and living standards.
More than mottos like zero tolerance, silica hazards
require multidisciplinary research, ranging from bench
to bedside, to socioecological health inequalities, and
attentive health surveillance able to detect continuously
renewed risks caused by this ubiquitous airborne
contaminant.
*†Catherine Cavalin, †Alain Lescoat, Alice Ballerie,
Nicolas Belhomme, Patrick Jégo, Stéphane Jouneau,
Valérie Lecureur, Mathieu Lederlin, Christophe Paris,
Paul-André Rosental
Interdisciplinary Research Institute for the Social Sciences,
National Centre for Scientific Research-National Institute for
Promoting clean air: combating fake news and denial
A fierce debate about the health effects of air pollution
erupted in the German media early this year. The scientific
evidence that links ambient air pollution—in particular,
fine particles (PM2.5; particles smaller than 2·5 µm) and
nitrogen dioxide (NO2)—to disease and mortality1,2 was
questioned by a small group of lung physicians and
engineers. They called to lift the limit values of ambient
elxeneize\iStockPhoto
particulate matter and NO2 concentrations in Europe,
claiming scarcity of evidence for such limits.3 Their
claims—broadly covered by German mainstream media
Published Online and social media—were welcomed by some politicians,
June 17, 2019
http://dx.doi.org/10.1016/
industry organisations, and members of the general
S2213-2600(19)30182-1 public. NO2 emissions were a focus of this debate because
traffic restrictions have been issued in many German cities
as a result of non-compliance with European Union limits.
650 www.thelancet.com/respiratory Vol 7 August 2019
Agricultural Research 7170-1427, Paris-Dauphine University,
75775 Paris, France (CC); Rennes 1 University, Rennes, France
(AL, AB, NB, PJ, SJ, VL, ML,CP); Centre for History at Sciences Po,
Sciences Po, Paris, France (P-AR)
catherine.cavalin@dauphine.psl.eu
†Contributed equally
We declare no competing interests.
1 Collis EL, Yule GU. The mortality experience of an occupational group
exposed to silica dust, compared with that of the general population and
of an occupational group exposed to dust not containing silica.
J Indust Hygiene 1933; 15: 395–417.
2 Editorial. The world is failing on silicosis. Lancet Respir Med 2019; 7: 283.
3 Shtraichman O, Blanc PD, Ollech J, et al. Outbreak of autoimmune disease
in silicosis linked to artificial stone. Occupl Med (Lond) 2015; 65: 444–50.
4 Webber M, Moir W, Crowson C, et al. Post-September 11, 2001, incidence
of systemic autoimmune diseases in World Trade Center-exposed
firefighters and emergency medical service workers. Mayo Clin Proc 2016;
91: 23–32.
5 Proctor RN, Schiebinger LL. The making and unmaking of ignorance.
Stanford University Press. Stanford; 2008.
6 Rosental P-A. Truncating a disease. The reduction of silica hazards to
silicosis at the 1930 International Labor Office conference on silicosis in
Johannesburg. Am J Ind Med 2015; 58: S6–14.
7 International Agency for Research on Cancer. Silica Dust, cristalline, in the
form of quartz or cristobalite. Monographs on the evaluation of carcinogenic
risks to humans. World Health Organization Press: Geneva, 2012.
8 European Union. Directive (EU) 2017/2398 of the European Parliament and
of the Council of 12 December 2017 amending Directive 2004/37/EC on the
protection of workers from the risks related to exposure to carcinogens or
mutagens at work. 2017. https://eur-lex.europa.eu/legal-content/EN/TXT/
PDF/?uri=CELEX:32017L2398&from=FR (accessed May 11, 2019).
9 Musu T. Revision of the Carcinogens Directive: anything happening?
HesaMag 2013; 8: 21–24.
10 Khamis W, Freynet O, Sesé L, Bernaudin J, Nunes H. Prognostic impact of
mediastinal lymph nodes in interstitial lung diseases: is environmental
exposure the offender? Am J Respir Crit Care Med 2019; 199: 1040–41.
11 Cavalin C. Exposome et sciences sociales: la promesse d’une rencontre?
Encyclopédie de l’environnement. 2018. https://www.encyclopedie-
environnement.org/societe/exposome-sciences-sociales-rencontre/
(accessed May 11, 2019).
Ambient air quality has improved substantially over
the past five decades as emission control, efficient
combustion engines, and cleaner fossil fuels have
been introduced in all sectors, including energy,
manufacturing, transport, and residential heating.
However, urban areas with heavy traffic remain hot
spots for particulate matter and NO2 across Europe.4
PM2·5, ozone, and NO2 affect the health of populations
around the globe.1 The effects start in the airways
and the lung, but air pollution affects the entire
body by inducing inflammatory systemic responses.5
Consequently, air pollution has been associated with
increased incidence of respiratory and cardiovascular
diseases and reduced life expectancy.5 Furthermore,
adverse effects on fetal development during pregnancy,