Atmospheric chemistry: Are plant emissions green?

Hydrocarbon emissions from living vegetation are thought to be harmful to the atmosphere. But the latest study suggests that the negative impact of these emissions in pristine environments is less than expected.

Do trees produce more pollution than cars? Terrestrial vegetation produces copious quantities of hydrocarbons and other volatile organic compounds (VOCs) that dominate global gas emissions. The largest component of emissions from vegetation is the hydrocarbon isoprene. Current models suggest that isoprene emissions in pristine environments can overwhelm the ability of atmospheric oxidants to remove 'greenhouse' gases (such as methane) and toxic gases (such as carbon monoxide). Furthermore, in a polluted atmosphere, isoprene emissions can substantially increase the amount of smog. But on page 737, Lelieveld et al. 1 propose that isoprene emitted by terrestrial ecosystems into unpolluted atmospheres is much less deleterious than was previously thought. Only when it comes into contact with air tainted by human activities does it exert a negative influence.
Some VOCs are known to attract pollinators and repel pests, but the function of isoprene remains a mystery, despite its prevalence in biogenic emissions. What was thought to be known was the dramatic negative impact of isoprene on chemical reactions in the troposphere -the lowest part of Earth's atmosphere.
The first speculation that abundant hydrocarbon emissions could modify atmospheric composition appeared almost 50 years ago 2 . Modern atmospheric-chemistry model (ACM) simulations now suggest that, in unpolluted air, isoprene depletes the levels of hydroxyl radicals ( • OH). Although these radicals are present in the atmosphere in minuscule amounts (less than 1 part per trillion), they are extremely reactive and serve as the primary cleansing agent for the atmosphere. In an atmosphere depleted of • OH, many trace gases would build up to dangerous levels.
Outside urban areas, isoprene is often the dominant reactive-gas emission, and so the typical fate for an • OH molecule in a clean atmosphere is removal by reaction with isoprene. Recent field studies in the remote Amazon basin have provided indirect evidence that isoprene has a considerably smaller effect on • OH than was previously thought 3,4 . Lelieveld et al. 1 now confirm this with direct measurements of • OH over the tropical rainforest in Suriname, Guyana and French Guiana. To explain their puzzling observation, the authors propose the existence of a previously overlooked reaction pathway that allows • OH consumed by isoprene to be directly recycled, so minimizing net • OH depletion. By setting the • OH recycling rate to a very high value in a modified ACM, they reproduced observed • OH levels over the rainforest.
Prior to this work 1 , there were already indications that something was amiss with the isoprene reactions used in ACMs for pristine atmospheres. For example, the atmospheric isoprene concentrations at several Amazonian sites were found to be lower than expected from the isoprene emissions measured at leaf-level, and from estimates of local • OH concentrations made using a detailed chemistry model 5 . A quick fix could be obtained by lowering the isoprene emission rates used in the model to agree with ambient concentration measurements.
But even these relatively low emission rates were not low enough for global ACMs, which have simplified chemistry models. In those ACMs, such emission rates caused a dramatic depletion of predicted • OH; this in turn leads to unrealistically high predictions of certain key atmospheric constituents. Most global modellers resolve this problem by using isoprene emission rates that are lower than Pristine rainforest in French Guiana. Global hydrocarbon emissions from tropical rainforests exceed those from cars.
estimates based on direct emission measurements, and lower than estimates based on the models used for local environments, but that are still within the range of uncertainty 6,7 . A promising approach for developing global maps of isoprene emissions is to make satellite observations of isoprene-oxidation products 8 , but this requires an accurate understanding of isoprene-oxidation processes. The inability of ACMs to incorporate measured isoprene emission rates is not limited to simulations of the undisturbed tropics. Air-quality modellers at US regulatory agencies have also had to decide between using isoprene emission rates based on measurements, or using inaccurate, substantially reduced emission rates that improve the ability of their model to simulate the actual distribution of oxidants 9 . Those modellers opted for the second approach. This might mean that they get the right answers for the wrong reason, but with pressing deadlines for regulatory decisions, they don't have time to wait for scientists to thrash out all the necessary details. Nevertheless, Lelieveld and colleagues' findings 1 should stimulate a re-evaluation of current predictive methods, in which the accuracies of the individual components of an ACM are considered afresh.
None of the recent field campaigns 1,3,4 that looked at isoprene oxidation over remote tropical forests has quantified all of the variables required to adequately constrain model simulations. Lelieveld and colleagues' measurements of • OH concentration are an invaluable step in the right direction, but simultaneous studies of • OH and isoprene fluxes, and of a more comprehensive suite of radicals and isoprene-oxidation products, are also needed. And as the authors point out, laboratory studies of isoprene-oxidation pathways will be essential to understand the processes maintaining • OH levels over tropical forests.
Field studies in less pristine regions are also required to determine whether such oxidation processes are relevant outside Earth's few remaining unpolluted locations. This could lead to a better understanding of the effect of airquality degradation on the chemical interactions between the biosphere and the atmosphere, and perhaps strengthen arguments for controlling emissions of atmospheric pollutants.

The generation of blood cells is a complex affair. As the culmination of several years of study by various investigators, the latest research will necessitate revision of textbook accounts of the process.
Red cells, white cells and platelets -on the face of it, the main components of blood look simple enough. All of them are ultimately produced from a common source, haematopoietic stem cells. And the white cells, or leukocytes, have a common general function, that of immune defence. But compared with red cells and platelets, leukocytes come in a large variety of specialized types, produced by a still somewhat mysterious variety of intermediate progenitor cells.
On pages 764 and 768 of this issue, Bell and Bhandoola 1 and Wada et al. 2 provide definitive evidence that a central aspect of blood-cell differentiation requires a rethink. Taken together with preceding work, their results show that a previously well-recognized distinction between two developmental lineages -lymphoid and myeloid -does not apply. But to appreciate this news, more details about each of the players and their function are required.
Immune cells are devoted to innate or to adaptive immunity. Components of the innate immune system are natural killer (NK) cells, monocytes/macrophages, granulocytes (a classification that includes neutrophils, eosinophils and basophils), mast cells and dendritic cells. The two arms of adaptive immunity are antibody-producing B cells and two types of T cell, cytotoxic and helper, which are respectively characterized by CD8 and CD4 cellsurface proteins. The well-established thinking has been that, along with NK cells, B and T cells are products of the lymphoid haematopoietic lineage, with all the others -including red cells and platelets -forming from the myeloid lineage. Most blood-cell production occurs in the bone marrow, with the exception of T cells, which originate in the bone marrow but mature in the thymus, a small organ in the upper chest.
The basis for the well-established picture stems from 1997, when a common lymphoid progenitor (CLP) was described 3 ; this progenitor could give rise to B and T cells as well as NK cells, but not to the myeloid lineage. A few years later the same investigators identified 4 a common myeloid progenitor (CMP), resulting in a haematopoietic tree that symmetrically branches into lymphoid and myeloid cells; this became the classic scheme of haematopoietic differentiation (Fig. 1). A prediction of this scheme was that CLPs migrate from the bone marrow to the thymus to initiate T-cell development. But this concept was subsequently challenged when it was reported that the predominant thymus-seeding cells do not resemble CLPs but have the characteristics of earlier haematopoietic progenitors 5 .
T-cell development in the thymus is astonishingly complex, occurring in up to nine sequential stages 6 that are identified by differences in gene expression and developmental potential. The stages can be simplified into the following succession: early T-cell progenitors (ETP, also called double-negative 1, or DN1, cells); DN2 and DN3 cells; CD4/CD8 double-positive cells; and finally CD4 or CD8 single-positive T cells. The various stages are orchestrated by the different microenvironments to which the cells become exposed as they migrate through the thymus 7 .
At which stage do thymic T-cell precursors lose their capacity to differentiate into alternative cell types? In line with the CLP model, mice in which the powerful T-cell regulator Notch1 was inhibited showed an increase in the number of thymic B cells but apparently not of myeloid cells (reviewed in refs 6 and 8). Against the model were several reports showing